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白芍提取物减轻链脲佐菌素诱导的糖尿病小鼠高血糖诱导的氧化应激和细胞凋亡的治疗潜力。

Therapeutic Potential of L. in Attenuating Hyperglycemia-Induced Oxidative Stress and Apoptosis in Alloxan-Administered Diabetic Mice.

机构信息

Department of Biochemistry, North Eastern Hill University, 793022 Shillong, Meghalaya, India.

Amity Institute of Biotechnology, Amity University Jharkhand, 834002 Ranchi, India.

出版信息

Front Biosci (Landmark Ed). 2023 May 26;28(5):105. doi: 10.31083/j.fbl2805105.

Abstract

BACKGROUND

Hyperglycemia-induced oxidative stress accelerates the process of apoptosis in tissues. (DI) is a medicinal plant, and its fruit contains many therapeutic properties. The therapeutic activity of the Methanolic Fruit Extract (MFE) of DI in attenuating oxidative stress and apoptosis in the liver and kidney tissues of alloxan-induced diabetic mice was analyzed in the present study.

METHODS

High-Performance Thin Layer Chromatography (HPTLC) profiling of MFE was conducted. GLUT4 protein expression analysis and lipid peroxidation assays were conducted to check for MFE effect by administering in diabetic mice. An ultrastructural study was conducted for both the tissues. In apoptotic studies, the TUNEL assay and apoptotic protein expression analysis was conducted.

RESULTS

High-Performance Thin Layer Chromatography (HPTLC) profiling of MFE showed the presence of two crucial antioxidants, ascorbic acid, and naringenin. In GLUT-4 protein expression analysis, MFE suppresses hyperglycemia by upregulating GLUT4 protein expression. Lipid peroxidation assay showed a decrease in malondialdehyde (MDA) upon MFE administration in diabetic mice. An ultrastructural study was conducted, and MFE was found to restore cellular alterations in diabetic tissues. In apoptotic studies, the TUNEL assay shows that MFE treatment showed fewer apoptotic cells than the diabetic group. The study also observed decreased caspase 3 protein expression and increased Bcl-2 protein expression.

CONCLUSIONS

Therefore, it is inferred from the study that MFE can exert a protective effect by suppressing hyperglycemia and modulating oxidative stress and apoptosis in alloxan-administered diabetic mice.

摘要

背景

高血糖诱导的氧化应激加速了组织细胞的凋亡过程。(DI)是一种药用植物,其果实含有许多治疗特性。本研究分析了 DI 的甲醇提取物(MFE)在减轻链脲佐菌素诱导的糖尿病小鼠肝、肾组织氧化应激和细胞凋亡中的治疗作用。

方法

采用高效薄层色谱(HPTLC)对 MFE 进行分析。通过在糖尿病小鼠中给药,检查 GLUT4 蛋白表达分析和脂质过氧化测定,以检查 MFE 的作用。对两种组织进行超微结构研究。在凋亡研究中,进行 TUNEL 检测和凋亡蛋白表达分析。

结果

MFE 的高效薄层色谱(HPTLC)分析显示存在两种重要的抗氧化剂,抗坏血酸和柚皮素。在 GLUT-4 蛋白表达分析中,MFE 通过上调 GLUT4 蛋白表达抑制高血糖。脂质过氧化测定显示,糖尿病小鼠给予 MFE 后丙二醛(MDA)减少。进行超微结构研究,发现 MFE 可恢复糖尿病组织中的细胞改变。在凋亡研究中,TUNEL 检测显示 MFE 处理组的凋亡细胞少于糖尿病组。该研究还观察到 caspase 3 蛋白表达减少和 Bcl-2 蛋白表达增加。

结论

因此,从研究中推断出 MFE 可以通过抑制高血糖和调节氧化应激和细胞凋亡来发挥保护作用,在链脲佐菌素给药的糖尿病小鼠中。

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