Publications by authors named "Jianhang Cai"

Article Synopsis
  • The study explored how polyphenols from the fruit of Phyllanthus emblica Linn. inhibit the enzyme acetylcholinesterase (AChE) using various methods including interaction assays and molecular simulations.
  • Key active compounds identified were myricetin, quercetin, fisetin, and gallic acid, which showed strong inhibition abilities, with myricetin being the most potent.
  • The findings highlighted that these polyphenols not only bind to AChE in different ways (competitive vs. non-competitive) but also cause structural changes in the enzyme, suggesting their potential as natural AChE inhibitors for further research.
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L. (PE) is commonly known as a medicine and food homologous plant, which is abundant in natural products polyphenols. In the present study, polyphenols were extracted from PE fruit by response surface method, and the anti-aging ability was determined.

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Objective: Astragaloside IV shows neuroprotective activity, but its mechanism remains unclear. To investigate whether astragaloside IV protects from endoplasmic reticulum stress (ERS), we focus on the regulation of glycogen synthase kinase-3 (GSK-3) and mitochondrial permeability transition pore (mPTP) by astragaloside IV in neuronal cell PC12.

Methods And Results: PC12 cells treated with different concentrations of ERS inductor 2-deoxyglucose (2-DG) (25-500 M) showed a significant increase of glucose-regulated protein 78 (GRP 78) and GRP 94 expressions and a decrease of tetramethylrhodamine ethyl ester (TMRE) fluorescence intensity and mitochondrial membrane potential (∆m), with the peak effect seen at 50 M, indicating that 2-DG induces ERS and the mPTP opening.

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This study investigates whether inhibition of endoplasmic reticulum (ER) stress prevents opening of the mitochondrial permeability transition pore (mPTP) and evaluates the corresponding signaling pathways involved in this process. Exposure of cardiac H9c2 cells to 800 µM HO for 20 min opened mPTP in response to oxidative stress, as demonstrated by quenching of tetramethylrhodamine ethyl ester (TMRE) fluorescence. Oxidative stress-induced mPTP opening was rescued by the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) in a dose-dependent manner at low concentrations.

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