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Berberine regulates mesangial cell proliferation and cell cycle to attenuate diabetic nephropathy through the PI3K/Akt/AS160/GLUT1 signalling pathway.
Ni, Wei-Jian; Guan, Xi-Mei; Zeng, Jing; Zhou, Hong; Meng, Xiao-Ming; Tang, Li-Qin.
  • Ni WJ; Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, The Key Laboratory of Anti-inflammatory of Immune Medicines (Ministry of Education), Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, Anhui, China.
  • Guan XM; Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
  • Zeng J; Anhui Provincial Hospital, Anhui Medical University, Hefei, Anhui, China.
  • Zhou H; Anhui Provincial Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
  • Meng XM; Anhui Provincial Hospital, Anhui Medical University, Hefei, Anhui, China.
  • Tang LQ; Department of Pharmacy, Anhui Provincial Cancer Hospital, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
J Cell Mol Med ; 26(4): 1144-1155, 2022 02.
Article in English | MEDLINE | ID: covidwho-1685345
ABSTRACT
High glucose (HG) is one of the basic factors of diabetic nephropathy (DN), which leads to high morbidity and disability. During DN, the expression of glomerular glucose transporter 1 (GLUT1) increases, but the relationship between HG and GLUT1 is unclear. Glomerular mesangial cells (GMCs) have multiple roles in HG-induced DN. Here, we report prominent glomerular dysfunction, especially GMC abnormalities, in DN mice, which is closely related to GLUT1 alteration. In vivo studies have shown that BBR can alleviate pathological changes and abnormal renal function indicators of DN mice. In vitro, BBR (30, 60 and 90 µmol/L) not only increased the proportion of G1 phase cells but also reduced the proportion of S phase cells under HG conditions at different times. BBR (60 µmol/L) significantly reduced the expression of PI3K-p85, p-Akt, p-AS160, membrane-bound GLUT1 and cyclin D1, but had almost no effect on total protein. Furthermore, BBR significantly declined the glucose uptake and retarded cyclin D1-mediated GMC cell cycle arrest in the G1 phase. This study demonstrated that BBR can inhibit the development of DN, which may be due to BBR inhibiting the PI3K/Akt/AS160/GLUT1 signalling pathway to regulate HG-induced abnormal GMC proliferation and the cell cycle, supporting BBR as a potential therapeutic drug for DN.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Berberine / Diabetes Mellitus / Diabetic Nephropathies Limits: Animals Language: English Journal: J Cell Mol Med Journal subject: Molecular Biology Year: 2022 Document Type: Article Affiliation country: Jcmm.17167

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Berberine / Diabetes Mellitus / Diabetic Nephropathies Limits: Animals Language: English Journal: J Cell Mol Med Journal subject: Molecular Biology Year: 2022 Document Type: Article Affiliation country: Jcmm.17167