Beneficial effects of procyanidin B2 on adriamycin-induced nephrotic syndrome mice: the multi-action mechanism for ameliorating glomerular permselectivity injury was written by Zhao, Chuanping;Tang, Jiamei;Li, Xiaoya;Yan, Zihan;Zhao, Liangliang;Lang, Wenbo;Yuan, Chunmao;Zhou, Chengyan. And the article was included in Food & Function in 2022.Electric Literature of C30H26O12 The following contents are mentioned in the article:
Despite considerable advances in prevention, diagnosis, and therapy, nephrotic syndrome (NS) remains a significant cause of high morbidity and mortality globally. As a result, there is an urgent need to identify novel effective preventative and therapeutic agents for NS. NS is implicated in glomerular permselectivity injury, which can be attributed to oxidative distress, inflammation, lipid nephrotoxicity, podocyte apoptosis, autophagy dysfunction, and slit diaphragm (SLD) dysfunction. In addition to its well-documented antioxidant potency, procyanidin B2 (PB2) may exhibit pleiotropic effects by targeting various canonical signaling events, such as NF-κB, PPARs, PI3K/Akt, mTOR, and the caspase family. As a result, PB2 may be a promising therapeutic target against NS. To test this hypothesis, we established an Adriamycin (ADR)-induced NS mouse model to evaluate the pleiotropic renoprotective effects of PB2 on NS. Here, we demonstrated that PB2 improves podocyte injury via inhibition of NOX4/ROS and Hsp90/NF-κB to exhibit antioxidant and anti-inflammatory potency, resp. We also show that PB2 indirectly activates the PI3K/Akt axis by regulating SLD protein levels, resulting in normalized podocyte apoptosis and autophagy function. Further, loss of albumin (ALB) induces lipid nephrotoxicity, which we found to be alleviated by PB2 via activation of PPARα/β-mediated lipid homeostasis and the cholesterol efflux axis. Interestingly, our results also suggested that PB2 reduces electrolyte abnormalities and edema. In addition, PB2 may contribute protective effects against trace element dys-homeostasis, which, through alleviating serum ALB loss, leads to a protective effect on glomerular permselectivity injury. Taken together, our results reveal that the identified mechanisms of PB2 on NS are multifactorial and involve inhibition of oxidative distress and inflammatory responses, as well as improvements in podocyte apoptosis and autophagy dysfunction, amelioration of lipid nephrotoxicity, and modulation of electrolyte abnormalities and edema. Thus, we provide a theor. basis for the clin. application of PB2 against NS. This study involved multiple reactions and reactants, such as (2R,2’R,3R,3’R,4R)-2,2′-Bis(3,4-dihydroxyphenyl)-[4,8′-bichromane]-3,3′,5,5′,7,7′-hexaol (cas: 29106-49-8Electric Literature of C30H26O12).
(2R,2’R,3R,3’R,4R)-2,2′-Bis(3,4-dihydroxyphenyl)-[4,8′-bichromane]-3,3′,5,5′,7,7′-hexaol (cas: 29106-49-8) belongs to alcohols. The oxygen atom of the strongly polarized O―H bond of an alcohol pulls electron density away from the hydrogen atom. This polarized hydrogen, which bears a partial positive charge, can form a hydrogen bond with a pair of nonbonding electrons on another oxygen atom. The most common reactions of alcohols can be classified as oxidation, dehydration, substitution, esterification, and reactions of alkoxides.Electric Literature of C30H26O12
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Alcohols – Chemistry LibreTexts