期刊
ANTIOXIDANTS
卷 12, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/antiox12061220
关键词
autophagy; AMPK; mTOR; Bclin-1; liposomal berberine; ER stress; type 2 diabetes
In this study, Lip-BBR was found to have beneficial effects in improving hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in T2DM. The treatment restored liver tissue microarchitectures, reduced steatosis and liver function, and promoted autophagy through the activation of LC3-II and Bclin-1 proteins and the AMPK/mTOR pathway. Additionally, Lip-BBR activated GLP-1 expression, decreased endoplasmic reticulum stress, oxidative stress, and inflammation.
In the advanced stages of type 2 diabetes mellitus (T2DM), diabetic liver damage is a common complication that can devastate a patient's quality of life. The present study investigated the ability of liposomal berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM) and the possible pathways by which it does so. Liver tissue microarchitectures and immunohistochemical staining were applied during the study. The rats were divided into a control non-diabetic group and four diabetic groups, which are the T2DM, T2DM-Lip-BBR (10 mg/kg b.wt), T2DM-Vildagliptin (Vild) (10 mg/kg b.wt), and T2DM-BBR-Vild (10 mg/kg b.wt + Vild (5 mg/kg b.wt) groups. The findings demonstrated that Lip-BBR treatment could restore liver tissue microarchitectures, reduce steatosis and liver function, and regulate lipid metabolism. Moreover, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats. Lip-BBR also activated the GLP-1 expression, which stimulated insulin biosynthesis. It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation. Collectively, Lip-BBR ameliorated diabetic liver injury in a T2DM rat model with its promotion activity of AMPK/mTOR-mediated autophagy and limiting ER stress.
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