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一种新型小檗碱制剂通过抑制磷脂酶 A/p38MAPK 通路保护胰岛细胞免于凋亡。

A New Berberine Preparation Protects Pancreatic Islet Cells from Apoptosis Mediated by Inhibition of Phospholipase A/p38 MAPK Pathway.

机构信息

Department of Pharmacology, School of Basic Medical Sciences, Jilin University, Changchun, China.

Department of Nephrology, China-Japan Union Hospital of Jilin University, Changchun, China.

出版信息

Bull Exp Biol Med. 2022 Jul;173(3):346-353. doi: 10.1007/s10517-022-05547-7. Epub 2022 Jul 19.

Abstract

We studied an amorphous solid dispersion of berberine with absorption enhancer sodium caprate (Huang-Gui solid dispersion preparations, HGSD). A therapeutic effect of HGSD was revealed in mice with type 2 diabetes mellitus and palmitate-induced injury to MIN6 β-cells. HGSD treatment (150 mg/kg) improved glucose metabolism and decreased β-cell apoptosis in diabetic mice. Furthermore, the effective component of HGSD berberine significantly attenuated the palmitate-induced decrease in MIN6 β-cells viability and insulin secretion. Moreover, molecular docking analysis and Western blotting showed that berberine decreased cell apoptosis and expression of group VIA phospholipase A (iPLA), p38 mitogen-activated protein kinase (p38 MAPK), and caspase-3. These data suggest that HGSD treatment protected β-cells via inhibiting the iPLA/p38 MAPK pathway.

摘要

我们研究了黄连素与吸收促进剂辛酸纳的无定形固体分散体(黄桂固体分散制剂,HGSD)。HGSD 在 2 型糖尿病小鼠和棕榈酸诱导的 MIN6 β 细胞损伤中显示出治疗效果。HGSD 治疗(150mg/kg)改善了糖尿病小鼠的葡萄糖代谢并减少了 β 细胞凋亡。此外,HGSD 中有效成分黄连素显著减轻了棕榈酸诱导的 MIN6 β 细胞活力和胰岛素分泌减少。此外,分子对接分析和 Western blot 表明,黄连素可减少细胞凋亡和表达组 VIA 磷脂酶 A(iPLA)、p38 丝裂原活化蛋白激酶(p38 MAPK)和半胱天冬酶-3。这些数据表明,HGSD 通过抑制 iPLA/p38 MAPK 通路来保护 β 细胞。

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