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贯叶连翘对糖尿病肥胖 db/db 小鼠胰岛素抵抗和氧化应激的改善作用。

Ameliorative effects of Penthorum chinense Pursh on insulin resistance and oxidative stress in diabetic obesity db/db mice.

机构信息

Department of Clinical Nutrition, The General Hospital of Western Theater Command, Chengdu, P. R. China.

School of Public Health, Southwest Medical University, Luzhou, P. R. China.

出版信息

PLoS One. 2024 Oct 7;19(10):e0311502. doi: 10.1371/journal.pone.0311502. eCollection 2024.

DOI:10.1371/journal.pone.0311502
PMID:39374222
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11458015/
Abstract

BACKGROUND

Penthorum chinense Pursh (PCP), a medicinal and edible plant, has been reported to protect against liver damage by suppressing oxidative stress. Type 2 diabetes mellitus (T2DM) is associated with liver dysfunction and oxidative stress. In the present study, we aim to investigate the hypoglycemic effect of PCP on db/db mice and further explore the underlying mechanisms.

METHODS

Thirty-two db/db mice were randomized into four groups, including a diabetic model control group (MC) and three diabetic groups treated with low (LPCP, 300 mg/kg/d), medium (MPLP, 600 mg/kg/d), and high doses of PCP (HPCP, 1200 mg/kg/d), and the normal control group (NC) of eight db/m mice were included. Mice in the NC and MC groups received the ultrapure water. After four weeks of intervention, parameters of fasting blood glucose (FBG), insulin resistance (IR), blood lipid levels, hepatic oxidative stress, and enzymes related to hepatic glucose metabolism were compared in the groups.

RESULTS

PCP administration significantly reduced FBG and IR in diabetic db/db mice, and improved hepatic glucose metabolism by increasing glucose transporter 2 (GLUT2) and glucokinase (GCK) protein expression. Meanwhile, PCP supplementation ameliorated hepatic oxidative stress by decreasing malonaldehyde content and increasing the activities of superoxide dismutase and glutathione peroxidase in db/db mice. Furthermore, PCP treatment reduced obesity and food intake in db/db mice, and improved dyslipidemia demonstrated by increasing high-density lipoprotein cholesterol (HDL-C) while decreasing total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (HDL-C). All doses of PCP treatment decreased the values of LDL-C/HDL-C in a dose-response relationship.

CONCLUSION

PCP significantly alleviated hyperglycemia, hyperinsulinemia, hyperlipidemia, and obesity, inhibited hepatic oxidative stress, and enhanced hepatic glucose transport in T2DM mice. Based on the above findings, the hypoglycemic effect of PCP may be attributed to the activation of the GLUT2/GCK expression in the liver and the reduction of hepatic oxidative stress.

摘要

背景

贯叶连翘(PCP)是一种药食同源植物,已被报道通过抑制氧化应激来保护肝脏免受损伤。2 型糖尿病(T2DM)与肝功能障碍和氧化应激有关。本研究旨在探讨 PCP 对 db/db 小鼠的降血糖作用,并进一步探讨其潜在机制。

方法

将 32 只 db/db 小鼠随机分为四组,包括糖尿病模型对照组(MC)和 3 个低剂量(LPCP,300mg/kg/d)、中剂量(MPLP,600mg/kg/d)和高剂量 PCP(HPCP,1200mg/kg/d)治疗组,每组 8 只 db/m 正常对照组(NC)。NC 和 MC 组给予超纯水。干预 4 周后,比较各组空腹血糖(FBG)、胰岛素抵抗(IR)、血脂水平、肝氧化应激及与肝糖代谢相关酶的变化。

结果

PCP 给药可显著降低糖尿病 db/db 小鼠的 FBG 和 IR,通过增加葡萄糖转运蛋白 2(GLUT2)和葡萄糖激酶(GCK)蛋白表达改善肝糖代谢。同时,PCP 补充剂通过降低丙二醛含量和增加超氧化物歧化酶和谷胱甘肽过氧化物酶的活性来改善 db/db 小鼠的肝氧化应激。此外,PCP 治疗降低了 db/db 小鼠的肥胖和摄食量,通过增加高密度脂蛋白胆固醇(HDL-C)同时降低总胆固醇(TC)、甘油三酯(TG)和低密度脂蛋白胆固醇(HDL-C)改善了血脂异常。所有剂量的 PCP 治疗均呈剂量依赖性降低 LDL-C/HDL-C 值。

结论

PCP 可显著缓解 T2DM 小鼠的高血糖、高胰岛素血症、高血脂和肥胖,抑制肝氧化应激,增强肝葡萄糖转运。基于上述发现,PCP 的降血糖作用可能归因于肝脏 GLUT2/GCK 表达的激活和肝氧化应激的降低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/1230116e0245/pone.0311502.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/d92ca5a8e924/pone.0311502.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/7c441b2e4a17/pone.0311502.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/e6ad876f23dc/pone.0311502.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/aab360b14ae9/pone.0311502.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/1230116e0245/pone.0311502.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/d92ca5a8e924/pone.0311502.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/7c441b2e4a17/pone.0311502.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/e6ad876f23dc/pone.0311502.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/aab360b14ae9/pone.0311502.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78ef/11458015/1230116e0245/pone.0311502.g005.jpg

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