Tag: 300-400

Lei-gong-gen formula granule attenuates hyperlipidemia in rats via cGMP-PKG signaling pathway was written by Lan, Taijin;Li, Qiaofeng;Chang, Ming;Yin, Chunli;Zhu, Dan;Wu, Zheng;Li, Xiaolan;Zhang, Weiquan;Yue, Bangwen;Shi, Junlin;Yuan, Hebao;Su, Zhiheng;Guo, Hongwei. And the article was included in Journal of Ethnopharmacology in 2020.Recommanded Product: 524-12-9 The following contents are mentioned in the article:

Lei-gong-gen formula granule (LFG) is a folk prescription derived from Zhuang nationality, the largest ethnic minority among the 56 nationalities in China. It is composed of three herbs, namely Centella asiatica (L.) Urb., Eclipta prostrata (L.) L., Smilax glabra Roxb. It has been widely used as health protection tea for many years to prevent cardiovascular and cerebrovascular diseases such as hyperlipidemia and hypertension. This study validated the lipid-lowering effect of LFG in a hyperlipidemia rat model. Then we employed network pharmacol. and mol. biol. approach to identify the active ingredients of LFG, corresponding targets, and its anti-hyperlipidemia mechanisms. Hyperlipidemia rat model was established by feeding male Sprague-Dawley rats with high-fat diet for two weeks. LFG (two doses of 10 and 20 g/kg) was administered orally to hyperlipidemia rat model for 4 wk, twice per day. Serum levels of total cholesterol (TC), triglycerides (TG), low-d. lipoprotein cholesterol (LDL-C), high-d. lipoprotein cholesterol (HDL-C) were monitored in rats pre and post-treatment. Hematoxylin-eosin staining was applied to observe the pathol. and lipid accumulation of liver. We then performed network pharmacol. anal. to predict the ingredients, their associated targets, and hyperlipidemia associated targets. Pathway anal. with significant genes was carried out using KEGG pathway. These genes and proteins intersectioned between compound targets and hyperlipidemia targets were further verified with samples from hyperlipidemia rats treated with LFG using Real-time RT-PCR and Western Blot. LFG attenuated hyperlipidemia in rat model, and this was characterized with decreased serum levels of TC, LDL-C, liver wet weight, and liver index. LFG alleviated the hepatic steatosis in hyperlipidemia rats. Network pharmacol. anal. identified 53 bioactive ingredients from LFG formula (three herbs), which link to 765 potential targets. 53 Hyperlipidemia associated genes were retrieved from public databases. There were 10 common genes between ingredients-targets and hyperlipidemia associated genes, which linked to 20 bioactive ingredients. Among these 10 genes, 3 of them were validated to be involved in LFG’s anti-hyperlipidemia effect using Real-time RT-PCR, namely ADRB2 encoding beta-2 adrenergic receptor, NOS3 encoding nitric oxide synthase 3, LDLR encoding low-d. lipoprotein receptor. The cGMP-PKG signaling pathway was enriched for hyperlipidemia after pharmacol. network anal. with ADRB2, NOS3, and LDLR. Interestingly, expression of cGMP-dependent protein kinase (PKG) was downregulated in hyperlipidemia rat after LFG treatment. Mol. docking study further supported that ferulic acid, histidine, p-hydroxybenzoic acid, and linalool were potential active ingredients for LFG’s anti-hyperlipidemia effect. LC-MS/MS anal. confirmed that ferulic acid and p-hydroxybenzoic acid were active ingredients of LFG. LFG exhibited the lipid-lowering effect, which might be attributed to downregulating ADRB2 and NOS3, and upregulating LDLR through the cGMP-PKG signaling pathway in hyperlipidemia rat. Ferulic acid and p-hydroxybenzoic acid might be the underlying active ingredients which affect the potential targets for their anti-hyperlipidemia effect. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Recommanded Product: 524-12-9).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofuran is the “”parent”” of many related compounds with more complex structures. For example, psoralen is a benzofuran derivative that occurs in several plants. Substituted benzofurans find applications such as fluorescent sensors, oxidants, in drug discovery, and in another field of chemistry and agriculture.Recommanded Product: 524-12-9

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

Anti-perimenopausal osteoporosis effects of Erzhi formula via regulation of bone resorption through osteoclast differentiation: A network pharmacology-integrated experimental study was written by Qin, Xiao-yan;Niu, Zi-chang;Han, Xiao-ling;Yang, Yun;Wei, Qiu;Gao, Xiao-xue;An, Ran;Han, Li-feng;Yang, Wen-zhi;Chai, Li-juan;Liu, Er-wei;Gao, Xiu-mei;Mao, Hao-ping. And the article was included in Journal of Ethnopharmacology in 2021.Formula: C16H10O7 The following contents are mentioned in the article:

Erzhi formula (EZF) consists of Ecliptae herba (EH) and Fructus Ligustri Lucidi (FLL) at a ratio 1:1, and constitutes a well-known formula in China that is commonly used for treating menopausal diseases. In this study, we explored the pharmacol. actions and potential mol. mechanisms underlying EZFs action in preventing and treating osteoporosis. The active components and related targets of EZFs anti-osteoporotic effects were predicted by network pharmacol., and functional enrichment anal. was also performed. We then used an osteoporosis model of ovariectomized (OVX) mice to detect the effects of EZF on osteoporosis. The results from network pharmacol. identified a total of 10 active ingredients from EH and 13 active ingredients from FLL that might affect 65 potential therapeutic targets. GO enrichment anal. revealed that EZF affected bone tissue primarily via hormone (particularly estradiol)-related pathways and bone resorption by osteoclast differentiation. KEGG anal. demonstrated that bone-related factors such as Runt-related transcription factor 2 (Runx2), Ca2, estrogen receptor1 (ESR1), androgen receptors (AR), and TNFα served as the primary targets during osteoclastic differentiation. In vivo experiments showed that the formula significantly improved the diminution in estrogen and the subsequent uterine atrophy induced by ovariectomy (P < 0.01 or 0.05), implying that the EZF exerted its actions via regulation of estradiol and the nourishing effects of the uterus in OVX mice. Dual-energy X-ray absorptiometry and micro-CT showed that EZF significantly inhibited bone loss and improved bone micro-architecture by statistically increasing the number of bone trabeculae and decreasing the separation of bone trabeculae in OVX mice (P < 0.01 or 0.05); EZF also inhibited bone loss and enhanced bone-fracture load. Furthermore, we confirmed that EZF reduced the calcium concentrations, augmented protein and mRNA levels for Runx2 in the bone marrow, and reduced PPARγ levels. RANKL-a key downstream regulatory protein of many targets that was referred to in our results of network pharmacol. as being involved in the regulation of osteoclastogenesis-was significantly diminished by EZF; it also elevated OPG content. In addition, we used monocytes of bone-marrow origin to detect the effects of the potential components of EZF on osteoclast differentiation and found that wedelolactone, oleanolic acid, echinocystic acid, luteolin, and luteolin-7-o-glucoside significantly inhibited osteoclast differentiation from monocytes induced by 25 ng/mL MCSF and 50 ng/mL RANKL (P < 0.01 or 0.05). Our present study indicated that EZF significantly inhibited the bone loss induced by OVX in mice by its regulation of estradiol combined with the nourishing effect of the uterus, and that it also attenuated bone resorption by decreasing the RANKL/OPG ratio so as to inhibit osteoclast maturation. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Formula: C16H10O7).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Many natural or synthetic compounds containing benzofuran skeletons have been found to possess remarkable activity as agrochemicals and pharmaceuticals. As benzofurans are prone to undergo ring opening of the heterocycle, examples of reduction of this type of aromatics by using dissolving metals are rather scarce.Formula: C16H10O7

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

Fisetin supplementation prevents high fat diet-induced diabetic nephropathy by repressing insulin resistance and RIP3-regulated inflammation was written by Ge, Chenxu;Xu, Minxuan;Qin, Yuting;Gu, Tingting;Lou, Deshuai;Li, Qiang;Hu, Linfeng;Nie, Xuyuan;Wang, Mingxing;Tan, Jun. And the article was included in Food & Function in 2019.Safety of 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one The following contents are mentioned in the article:

Obesity-related renal disease is related to caloric excess promoting deleterious cellular responses. However, a full understanding of the mol. mechanisms involved in progressive kidney disease, as well as a therapeutic strategy, is still absent. Fisetin (FIS), as a natural flavonoid, possesses various bioactivities in a number of disease models. However, its role in obesity-associated kidney injury is still unclear and requires elucidation. In our study, an obesity animal model was established using C57BL/6 mice fed with a normal chow diet (NCD) or high fat diet (HFD) for 16 wk with or without FIS administration (20, 40 or 80 mg kg^-1). Our results indicated that chronic HFD feeding led to a significant body weight gain in mice compared to the normal control group, accompanied by a marked insulin resistance and glucose intolerance, whereas FIS treatment exerted prominently protective effects. In addition, FIS significantly attenuated HFD-induced histol. alterations in renal tissue samples. Moreover, FIS treatment down-regulated expression of kidney injury mol.-1 (KIM-1), and up-regulated nephrin and podocin expression levels in the kidneys of HFD-fed mice, improving their renal dysfunction. After HFD feeding, mice treated with FIS exhibited a decrease in phosphorylated IRS1^Ser307, and an increase in phosphorylated glycogen synthase kinase 1 (IRS1^Tyr608), AKT, forkhead box protein O1 (FOXO1) and glycogen synthase kinase (GSK)-3β. Furthermore, FIS administration markedly restrained the inflammatory response in the kidneys of HFD-challenged mice, as evidenced by the reduced pro-inflammatory cytokines, tumor necrosis factor- α (TNF- α), interleukin 6 (IL-6), IL-1β and IL-18, which was attributed to the blockage of nuclear factor κ B (NF-κ B) signaling. Importantly, FIS-treated obese mice exerted a remarkable decrease in RIP3 expressions in the kidneys compared to obese mice in the absence of FIS, along with an evident reduction in the NOD-like receptor protein 3 (NLRP3), an apoptosis-associated speck-like protein containing a Caspase recruitment domain (ASC) and Caspase-1. The protective effects of FIS against HFD-induced renal injury were verified in vitro using palmitate (PAL)-treated HK2 cells, an immortalized proximal tubule epithelial cell line from the adult human kidney. In summary, our results supported the notion that FIS functions as a promising agent to improve insulin resistance and inflammatory response against metabolic stress-induced renal injury. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Safety of 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofurans are only weakly aromatic in nature and they are cleaved by many oxidative and reductive conditions. Benzofurans have also made significant and distinctive contributions to biology. They exhibit several biological activities that range from antiviral, antimicrobial, antitumor, anti-inflammatory.Safety of 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

The traditional mongolian medicine qiqirigan-8 effects on lipid metabolism and inflammation in obesity: pharmacodynamic evaluation and relevant metabolites was written by Narenmandula;Hongmei;Ding, Xiaoqing;Li, Kexin;Hashentuya;Yang, Dezhi;Wendurige;Yang, Rui;Yang, Dandan;Tana;Wang, Haisheng;Eerdunduleng;Tegexibaiyin;Wang, Changshan;Bao, Xilinqiqige;Menggenduxi. And the article was included in Frontiers in Pharmacology in 2022.Application of 524-12-9 The following contents are mentioned in the article:

Traditional Mongolian Medicine Qiqirigan-8 (MMQ-8) is a Chinese botanical drug with effective pharmacol. properties in obesity. However, the pharmacol. mechanism of MMQ-8 remains unclear. This study aimed to determine the active metabolites of MMQ-8 and its therapeutic effects on lipid metabolism and inflammation. The active metabolites of MMQ-8 were identified by ultrahigh-performance liquid chromatograph Q extractive mass spectrometry (UHPLC-QE-MS) assay and network anal. An obesity rat model induced by high-fat diet was used in the study. Serum levels of lipids and inflammatory factors were detected using biochem. anal. and ELISA (ELISA). Pathol. anal. of liver tissues and arteries was conducted with hematoxylin and eosin (H&E) staining and immunohistochem. Protein expression of the tumor necrosis factor (TNF) signaling pathway was investigated by Western-blot. Simultaneously, bone marrow cells were used for RNA sequencing and relevant results were validated by cell culture and quant. real-time polymerase chain reaction (RT-qPCR). We identified 69 active metabolites and 551 target genes of MMQ-8. Of these, there are 65 active metabolites and 225 target genes closely related to obesity and inflammation. In vivo, we observed that MMQ-8 had general decreasing effects on body weight, white adipose tissue weight, and serum lipids. MMQ-8 treatment notably decreased the liver function markers and hepatic steatosis, and significantly decreased inflammation. In serum, it notably decreased TNF-α, interleukin (IL)-6, and inducible nitric oxide synthase (INOS), while elevating IL-10 levels. MMQ-8 treatment also significantly inhibited proteins phosphorylation of nuclear factor-kappa B inhibitor alpha (IκBα), mitogen-activated protein kinase (p38), extracellular regulated kinase 1/2(ERK1/2), and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and decreased vascular endothelium damage and macrophage infiltration and polarization to M1. These findings coincide with the RNA-sequencing data of bone marrow cells and results of in vitro experiments We determined the pharmacol. actions and relevant metabolites of MMQ-8 in obesity for the first time. Our study revealed MMQ-8 can optimize lipid metabolism and reduce chronic inflammation in obesity. However, more in-depth research is needed, for example, to understand the principle of compound compatibility and the inhibition effects on hepatic steatosis, T cell differentiation, and inflammatory signal transduction. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Application of 524-12-9).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofuran is the “”parent”” of many related compounds with more complex structures. For example, psoralen is a benzofuran derivative that occurs in several plants. They are also prone to polymerisation in the presence of concentrated mineral acids and Lewis acids.Application of 524-12-9

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

Cucumis melo var. momordica as a Potent Antidiabetic, Antioxidant and Possible Anticovid Alternative: Investigation through Experimental and Computational Methods was written by Yadav, Jagat Pal;Grishina, Maria;Shahbaaz, Mohd;Mukerjee, Alok;Singh, Sunil Kumar;Pathak, Prateek. And the article was included in Chemistry & Biodiversity in 2022.Quality Control of 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one The following contents are mentioned in the article:

Diabetes mellitus is a typical life threatening of disease, which generate due to the dysfunction of β cells of pancreas. In 2014, WHO stated that 422 million people were infected with DM. The current pattern of management of diabetes included synthetic or plant based oral hypoglycemic drugs and insulin but drug resentence is become a very big issues in antidiabetic therapy. Thus, its very earnest to discover now medication for this disease. Now the days, it is well acknowledged that diabetic patients are more prone towards covid and related complications. Thus, medical practitioners reformed the methodol. of prescribing medication for covid infected antidiabetic therapy and encouraging the medication contains dual pharmacol. properties. It is also well know that polyphenols specifically hold a significant role in oxidative stress and reduced the severity of many inflammatory diseases. Cucumis melo has rich history as ethano-pharmacol. use in Indian subcontinent. The fruit and seed are well-known for the treatment of various diseases due to the presence of phenolics. Therefore, in this study, the combined mixture of flower and seeds were used for the extraction of polyphenolic rich extract and tested for antidiabetic activity through the antioxidant and in vivo experiments The antioxidant potential measurement exhibited that the selected plant extract has the significant competence to down-regulate oxidative stress (DPPH scavenging IC50 at 60.7±1.05 μg/mL, ABTS IC50 at 62.15±0.50 μg/mL). Furthermore, the major polyphenolic phyto-compounds derived from the Cucumis melo were used for in silico anticovid activity, docking, and complementarity studies. The anticovid activity prognosis reflected that selected phyto-compounds amentoflavone and vanillic acid have optimal possibility to interact with 3C-like protease and through this moderate anticovid activity can be exhibit. The docking experiments established that the selected compounds have propensity to interact with protein tyrosine phosphatase 1B, 11β-Hydroxysteroid dehydrogenase, superoxide dismutase, glutathione peroxidase, and catalase β-glucuronidase receptor. In vivo experiments showed that 500 mg/kg, Cucumis melo extract ominously amplified body weight, plasma insulin, high-d. lipoprotein levels, and biochem. markers. Furthermore, extract significantly downregulate the blood glucose, total cholesterol, triglycerides, low-d. lipoprotein, and very low-d. lipoprotein. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Quality Control of 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofurans are only weakly aromatic in nature and they are cleaved by many oxidative and reductive conditions. In nature, benzofurans have occupied an important role among the plant phenols & several pharmacologically active compounds.Quality Control of 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

corrected and Republished: Comparative botanical and phytochemical studies of ambiguous medicinal plant species of Wedelia and Eclipta (Fam. Asteraceae) used in ASU systems of medicine with special reference to in-silico screening of hepatoprotective potential of marker wedelolactone with acetaminophen targets was written by Arunachalam, C.;Arunadevi, R.;Murugammal, S.;Monika, N.;Susila, R.;Kumar, K. N. Sunil. And the article was included in Pharmacognosy Research in 2021.SDS of cas: 524-12-9 The following contents are mentioned in the article:

Context: In traditional medicine, Kesaraja (Ayurveda) or Manjal karisali (Siddha) is effective for jaundice. Aim: Three species of Asteraceae need to be studied for their therapeutic superiority of their intended claim. They are Wedelia chinensis (Osbeck) Merr. Philipp J., Wedelia trilobata (L.) Hitchc. and Eclipta prostrata (L.) L. (Asteraceae). The present study aimed to screen and characterize the potential species for therapeutic purpose. Materials and Methods: The whole plants, W. chinensis (Osbeck) Merr. W. trilobata (L.) Hitchc. and E. prostrata (L.) (Asteraceae) were collected and botanically identified. Preliminary phytochem. anal. and high-performance thin-layer chromatog. finger printing with marker wedelolactone were done for the ethanolic extracts of these plants. Botanical and pharmacognostical diagnostic characters of the plants based on macro-morphol., micro-morphol. and powder microscopical characterization were worked out. Comparative in-vitro antioxidant potential of ethanolic extracts of these plant species was carried out. Using ADMET SAR software, the pharmacokinetics of wedelolactone were predicted. Using Autodock 4.2 software, the binding energy of wedelolactone on targets of acetaminophen-induced hepatotoxicity namely PPAR-α, AMPK, JNK-1, EGFR, Nrf2, ALT, ALP, GGT, CAR, Frizzled receptor, FXR, ERK1, LXR, mitochondrial glutamate dehydrogenase, p53, mTOR C1, CYP1A2, CYP2E1, 5-lipoxygenase, thrombin, UCP1, GSK1, RXR and PXR was predicted. Results: All the three plant species were pharmacognostically and chem. different. W. chinensis was found to possess more antioxidant potential than the other two plants. The marker compound wedelolactone was not detected in W. trilobata. Wedelolactone passed the Lipinski′s rule of five, and the docking anal. of wedelolactone confirmed high binding affinity toward PPAR-α, AMPK, Nrf2, CYP2E1, EGFR, JNK1, UCP-2, thrombin, 5-lipoxygenase, mTORC1, RXR, FXR, LXR, Frizzled receptor, GDH and Erk-1. Conclusion: Based on the above observations, we conclude that the presence of marker compound wedelolactone might have attributed the potency of W. chinensis and E. prostrata in counteracting acetaminophen toxicity when compared with W. trilobata. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9SDS of cas: 524-12-9).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofurans are only weakly aromatic in nature and they are cleaved by many oxidative and reductive conditions. Benzofurans have also made significant and distinctive contributions to biology. They exhibit several biological activities that range from antiviral, antimicrobial, antitumor, anti-inflammatory.SDS of cas: 524-12-9

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

In silico analysis and identification of antiviral coumarin derivatives against 3-chymotrypsin-like main protease of the novel coronavirus SARS-CoV-2 was written by Abdizadeh, Rahman;Hadizadeh, Farzin;Abdizadeh, Tooba. And the article was included in Molecular Diversity in 2022.Formula: C16H10O7 The following contents are mentioned in the article:

Abstract: Coronavirus disease 2019 (COVID-19) is a pandemic viral disease caused by SARS-CoV-2 that generated serious damages for both the human population and the global economy. Therefore, it is currently considered as one of the most important global health problems of human societies and there is an urgent need for potent drugs or vaccines which can effectively combat this virus. The chymotrypsin-like protease (3CLpro) of SARS-CoV-2 plays a key role in the viral replication inside the host and thus is a promising drug target to design and develop effective antiviral drugs against SARS and other coronaviruses. This study evaluated some antiviral coumarin phytochems. as potential inhibitors of coronaviruses 3CLpro by in silico approaches such as mol. docking, ADMET prediction, mol. dynamics simulation, and MM-PBSA binding energy calculation Natural coumarin derivatives were docked to the 3CLpro of SARS-CoV-2 and for further investigation, docked to the 3CLpro of SARS-CoV and MERS-CoV. The docking scores of these natural compounds were compared with 3CLpro referenced inhibitors (ritonavir and lopinavir) and co-crystal inhibitor N3. Mol. docking studies suggested more than half of the coumarin phytochems. had favorable interaction at the binding pocket of the coronaviruses 3CLpro and exhibited better binding affinities toward 3CLpro than ritonavir and lopinavir. Most antiviral phytochems. interact strongly with one or both the catalytic dyad residues (His41 and Cys145) and the other key residues of SARS-CoV-2 main protease. Further, MD simulation and binding free energy calculations using MM-PBSA were carried out for three 3CLpro-coumarin complexes and 3CLpro-N3/lopinavir. The results confirmed that the 3CLpro-glycycoumarin, 3CLpro-oxypeucedanin hydrate, and 3CLpro-inophyllum P complexes were highly stable, experience fewer conformation fluctuations and share a similar degree of compactness. Also, the pharmacokinetics and drug-likeness studies showed good results for the selected coumarin phytochems. Therefore, the coumarin phytochems. could be used as antiviral agents in the treatment of COVID-19 after further studies. Graphical abstract: [graphic not available: see fulltext] This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Formula: C16H10O7).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives.Benzofuran is one of the most significant oxygen-containing heterocycles consisting of fused benzene and furan ring, which are widely presented in various naturally occurring and synthetically active compounds. Substituted benzofurans find applications such as fluorescent sensors, oxidants, in drug discovery, and in another field of chemistry and agriculture.Formula: C16H10O7

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

Enhanced Accumulation of Cisplatin in Ovarian Cancer Cells from Combination with Wedelolactone and Resulting Inhibition of Multiple Epigenetic Drivers. was written by Sarwar, Sadia;Alamro, Abir A;Alghamdi, Amani A;Naeem, Komal;Ullah, Salamat;Arif, Muazzam;Yu, Jun Qing;Huq, Fazlul. And the article was included in Drug design, development and therapy in 2021.HPLC of Formula: 524-12-9 The following contents are mentioned in the article:

PURPOSE: Cisplatin resistance is a major concern in ovarian cancer treatment. The aim of this study was to investigate if wedelolactone could perform better in resistant ovarian cancer cells when used in combination with cisplatin. METHODS: Growth inhibitory potential of wedelolactone and cisplatin was investigated through MTT reduction assay in ovarian cancer cell lines including A2780 (sensitive), A2780^cisR (cisplatin resistant) and A2780^ZD0473R. Resistance factor (RF) of drugs was determined in these three cell lines. Combination index (CI) was calculated as a measure of combined drug action. Effect of this combination on changes in the cellular accumulation of platinum levels and platinum-DNA binding was also determined in vitro using AutoDock Vina while the effect of wedelolactone on inhibition of possible key culprits of resistance including Chk1, CD73, AT tip60, Nrf2, Brd1, PCAF, IGF1, mTOR1 and HIF2α was investigated in silico. RESULTS: Cisplatin and wedelolactone showed a dose-dependent growth inhibitory effect. RF value of wedelolactone was 1.1 in the case of A2780^cisR showing its potential to bring more cell death in cisplatin-resistant cells. CI values were found to vary showing antagonistic to additive outcomes. Additive effect was observed for all sequences of administration (0/0, 0/4 and 4/0 h) in A2780^cisR. Enhanced cellular accumulation of cisplatin was observed in parent and resistant cells on combination. Docking results revealed that among the selected oncotargets, Chk1, CD73, Nrf2, PCAF and AT tip60 were more vulnerable to wedelolactone than their respective standard inhibitors. CONCLUSION: These findings have shown that additive outcome of drug combination in A2780^cisR and raised levels of platinum accumulation followed a clear pattern. This observation indicates that the presence of wedelolactone might have contributed to sensitize A2780^cisR. However, in silico results point to the possible effects of this compound on epigenetic factors involving tumor microenvironment, epithelial mesenchymal transition, and immune-checkpoint kinases. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9HPLC of Formula: 524-12-9).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofuran is the “”parent”” of many related compounds with more complex structures. For example, psoralen is a benzofuran derivative that occurs in several plants. Introduction of benzofurans in organic synthesis, particularly drug synthesis, involves generally the use of their metalated species as nucleophiles in addition reactions or in metal-catalysed cross-coupling reactions.HPLC of Formula: 524-12-9

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

Effect of wedelolactone and gallic acid on quinolinic acid-induced neurotoxicity and impaired motor function: significance to sporadic amyotrophic lateral sclerosis was written by S, Maya;T, Prakash;Goli, Divakar. And the article was included in NeuroToxicology in 2018.Reference of 524-12-9 The following contents are mentioned in the article:

Quinolinic acid (QUIN) is a well-known neuroactive metabolite of tryptophan degradation pathway or kynurenine pathway. The QUIN is involved in the development of several toxic cascades which leads to the neuronal degeneration processes. The QUIN-induced toxicity is also responsible for the impairment of the motor function and motor learning ability. This study seeks to investigate the several mechanisms which are involved in the intrastriatal administration of QUIN-induced neurodegeneration and the neuroprotective effects of wedelolactone (WL) and gallic acid (GA) over QUIN-induced toxicity. The Wistar rats were used for the study and conducted behavioral model to evaluate the effects of WL (100 & 200 mg/kg) and GA (100 & 200 mg/kg) on impaired motor function and motor learning ability. We also assessed the effects of WL and GA on the antioxidant profile, cytotoxicity, apoptosis, excitotoxicity, inflammatory cascades, and on growth factors which helps in neurogenesis. The compounds effectively improved the motor function, motor learning memory in the rats. Similarly, enhanced the activity of Glutathione peroxidase, SOD, catalase, and declined the lipid peroxidation and nitrite production in the brain. The treatment with WL and GA lowered the activities of LDH, m-calpain, and caspase-3. The reports strongly support that both compounds are useful in the prevention of glutamate excitotoxicity induced by QUIN. The NAA, IGF-1, and VEGF levels in the brain were improved after treatment with WL and GA. The neuroprotective effects of WL and GA further proved through the anti-inflammatory effects. The compounds significantly down-regulated the expression of TNF-α, IL-6, and IL-β in the brain. Immunohistochem. anal. shows that the WL and GA reduced the expression of NF-κB. The histopathol. studies for cerebellum, hippocampus, striatum, and spinal cord confirms the toxic effects of QUIN and neuroprotective effects of WL and GA. The results suggest that WL and GA could ameliorate the toxic events triggered by QUIN and might be effective in the prevention and progression of several cascades which lead to the development of sALS. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Reference of 524-12-9).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofuran derivatives are one of the most important oxygen-containing heterocycles. Benzofurans have also made significant and distinctive contributions to biology. They exhibit several biological activities that range from antiviral, antimicrobial, antitumor, anti-inflammatory.Reference of 524-12-9

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem

The combined effect of oleonuezhenide and wedelolactone on proliferation and osteoblastogenesis of bone marrow mesenchymal stem cells was written by Deng, Xue;Tan, Suming;Zhu, Di;Sun, Yujiao;Yu, Jinghua;Meng, Xiangling;Zheng, Luping;Liu, Yanqiu. And the article was included in Phytomedicine in 2019.Recommanded Product: 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one The following contents are mentioned in the article:

Regulation of the survival and differentiation of bone marrow mesenchymal stem cells is an essential consideration in the development of targeted drugs for treatment of osteoporosis. The present study aimed to evaluate the combined effect of wedelolactone and oleonuezhenide, two compounds from Chinese formula Er-Zhi-Wan, on osteoblastogenesis and the underlying mol. mechanisms. MTT assay was taken to evaluate cell proliferation. The alk. phosphatase (ALP) activity assay was used to determine the activity of ALP. Alizarin red S (ARS) staining was taken to indicate the intensity of the calcium deposits. Quant. real-time PCR and Western blot were performed to the levels of Runx2, Osteocalcin, and Osterix expression in mouse bone marrow mesenchymal stem cells (BMSCs). Ovariectomized mouse model and bone histomorphometric anal. were also used to research the effects of wedelolactone and oleonuezhenide on bone loss caused by ovariectomy. Wedelolactone combined with oleonuezhenide enhanced osteoblast differentiation and bone mineralization. Osteoblastogenesis-related marker genes including osteocalcin, Runx2, and osteorix were upregulated in the presence of wedelolactone and oleonuezhenide. At the mol. level, oleonuezhenide did not affect GSK-3β phosphorylation induced by wedelolactone, but elevated casein kinase 2-alpha (CK2α) expression, resulting in β-catenin and Runx2 nuclear translocation. In addition, 30μM wedelolactone-induced cytotoxicity in bone marrow mesenchymal stem cells was relieved by 9μM oleonuezhenide. These cells were protected by oleonuezhenide and maintained osteoblastic activity. Oleonuezhenide increased Wnt5a and CK2α expression. Wedelolactone-reduced extracellular signal-regulated kinase (ERK) phosphorylation was reversed by oleonuezhenide. In ovariectomized mice, administration of wedelolactone and oleonuezhenide prevented ovariectomy-induced bone loss by enhancing osteoblastic activity. These results suggested that oleonuezhenide enhanced the effects of wedelolactone on osteoblastogenesis. These two compounds could be developed as a combined therapeutic agent for osteoporosis. This study involved multiple reactions and reactants, such as 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9Recommanded Product: 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one).

1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one (cas: 524-12-9) belongs to benzofurans derivatives. Benzofurans are compounds with a planar structure having 10 pi electrons that include the lone pair on oxygen atom, which makes it more susceptible to electrophilic attack. They are also prone to polymerisation in the presence of concentrated mineral acids and Lewis acids.Recommanded Product: 1,8,9-Trihydroxy-3-methoxy-6H-benzofuro[3,2-c]chromen-6-one

Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem