ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2020
Yu Nu Compound Regulates Autophagy and Apoptosis Through mTOR in vivo and vitro.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Potential effect of tropical fruits Phyllanthus emblica L. for the prevention and management of type 2 diabetic complications: a systematic review of recent advances.European journal of nutrition · 2021Pooled it
- Bioinformatics Analysis and Experimental Findings Reveal the Therapeutic Actions and Targets ofJournal of diabetes research · 2024Article
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- The Role and Mechanism of Metformin in Inflammatory Diseases.Journal of inflammation research · 2023Review
- Mutation of Beclin1 acetylation site at K414 alleviates high glucose-induced podocyte impairment in the early stage of diabetic nephropathy by inhibiting hyperactivated autophagy.Molecular biology reports · 2022Article
- Traditional Chinese Medicine in Treating Primary Podocytosis: From Fundamental Science to Clinical Research.Frontiers in pharmacology · 2022Review
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8 authors at 1 institution in 1 country.
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Abstract
introductionYu Nu compound (YNJ) is a traditional Chinese medicine widely utilized to treat type 2 diabetes possibly through mediating autophagy. Abnormal podocyte autophagy and apoptosis could result in podocyte loss in diabetics nephropathy (DN). The mechanism of Yu Nu compound in DN is still unclear. Therefore, the study aims to investigate the effects of Yu Nu compound and analyze the potential mechanism.
methodsGoto-Kakizaki (GK) rats were administered using YNJ with different doses once a day by gavage for 4 weeks. The renal cortex injury was observed by HE staining and electron microscope. Cell apoptosis of renal cortex was analyzed by TUNNEL staining. The mTOR, autophagy-related proteins and apoptosis-related proteins were detected by Western blot or real-time PCR in vivo and vitro. MPC5 cells were exposed to high glucose (HG, 30mM) for 12h to simulate podocyte injury in DN. MPC5 cells were treated by serum containing YNJ with different dosages. Cell activities and apoptosis were, respectively, detected through Cell Counting Kit-8 (CCK8) assay and flow cytometry.
resultsThe results showed that the medium dose of YNJ had better effects on decreasing blood glucose and improving renal injury in GK rats, followed by decreasing mTOR levels. The autophagy levels were enhanced in renal cortex, accompanied with the increase of cell apoptosis in vivo. Besides, the proteins regulating autophagy and apoptosis were significantly modulated by YNJ in GK rats. Then, we found that the decreasing endogenous mTOR could reverse the effects of YNJ on podocyte apoptosis and autophagy in vivo. DISCUSSION: The study suggested that YNJ recovered normal autophagy and suppressed apoptosis through regulating mTOR. The maintenance of normal basal autophagic activity possibly based on the effect of YNJ on multiple target was essential for maintaining podocyte function.
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