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齐墩果酸通过减轻 STZ 诱导的高血糖小鼠胰岛氧化应激介导的炎症和细胞凋亡改善胰岛功能。

Amelioration of oxidative stress mediated inflammation and apoptosis in pancreatic islets by Lupeol in STZ-induced hyperglycaemic mice.

机构信息

Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata 700054, West Bengal, India.

Department of Biochemistry and Biophysics, University of Kalyani, Kalyani, 741235, Nadia, West Bengal, India.

出版信息

Life Sci. 2022 Sep 15;305:120769. doi: 10.1016/j.lfs.2022.120769. Epub 2022 Jul 2.

Abstract

BACKGROUND

Type 1 Diabetes mellitus initiates by loss of pancreatic activity which affects other major organs leading to multi-organ failure. Lupeol, a novel phytochemical, is emerging as a potent bioactive molecule. However, the effect of lupeol on hyperglycaemia is not clearly understood. This study delivers an elaborate vision towards the detailed molecular pathway of lupeol against STZ induced diabetic difficulties of the pancreas.

METHOD

The current experiments were designed to focus on the ameliorative effect of the triterpene in combating oxidative damage on the pancreas in a preclinical streptozotocin induced mouse model. After diabetic induction, the animals were subjected to administration with 75 mg kg body weight of lupeol, thrice a week for 7 weeks. Histological measurements were done to investigate the anatomy of the pancreas as well as molecular mechanisms were explored.

RESULTS

The compound was found to regulate several hyperglycaemic and oxidative stress related markers. Lupeol treatment also reversed the expression levels of inflammatory cytokines (TNF-α and IL-1β) as well as attenuated the NF-κB mediated inflammatory and extrinsic apoptotic pathway.

DISCUSSION

These findings in preclinical streptozotocin induced in vivo mouse model strongly suggest the discovery of novel properties of lupeol against oxidative stress in pancreatic β cells by regulating the NF-κB and extrinsic apoptotic pathway.

摘要

背景

1 型糖尿病由胰腺功能丧失引发,这会影响其他主要器官,导致多器官衰竭。羽扇醇,一种新型植物化学物质,正作为一种有效的生物活性分子出现。然而,羽扇醇对高血糖的影响尚不清楚。本研究深入探讨了羽扇醇针对 STZ 诱导的糖尿病胰腺损伤的详细分子途径。

方法

本实验旨在关注三萜在临床前链脲佐菌素诱导的小鼠模型中对抗胰腺氧化损伤的改善作用。糖尿病诱导后,动物每周接受 3 次 75mg/kg 体重的羽扇醇治疗,共 7 周。进行组织学测量以研究胰腺的解剖结构,并探讨分子机制。

结果

该化合物被发现可调节多种高血糖和氧化应激相关标志物。羽扇醇治疗还逆转了炎症细胞因子(TNF-α和 IL-1β)的表达水平,并减弱了 NF-κB 介导的炎症和外在细胞凋亡途径。

讨论

这些在临床前链脲佐菌素诱导的体内小鼠模型中的发现强烈表明,羽扇醇通过调节 NF-κB 和外在细胞凋亡途径,在胰腺β细胞中发现了针对氧化应激的新特性。

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