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桑约德大米提取物通过调节Akt/丝裂原活化蛋白激酶信号通路减轻糖尿病大鼠模型的血管炎症和损伤。

Sangyod Rice Extract Attenuates Vascular Inflammation and Injury in a Rat Model of Diabetes by Modulating the Akt/MAPK Signaling Pathway.

作者信息

Woonnoi Wanwipha, Thipart Kornsuda, Hanchang Wanthanee, Saetan Jirawat, Tanasawet Supita, Moolsup Furoida, Suttithumsatid Wiwit, Wongtawatchai Tulaporn, Sukketsiri Wanida

机构信息

Division of Health and Applied Sciences, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla 90110, Thailand.

Department of Physiology, Faculty of Medical Science, Naresuan University, Muang, Phitsanulok 65000, Thailand.

出版信息

Adv Pharmacol Pharm Sci. 2025 Apr 17;2025:1169062. doi: 10.1155/adpp/1169062. eCollection 2025.

DOI:10.1155/adpp/1169062
PMID:40276785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12021485/
Abstract

Our previous study has shown the beneficial effect of the ethanolic extract of Sangyod rice (SE) on lipid accumulation and insulin resistance. However, its effect on vascular inflammation has yet to be explored. The current study aimed to investigate the anti-inflammatory effects of SE in both in vitro and in vivo models, specifically examining its impact on LPS-induced inflammation in RAW264.7 cells and evaluating its efficacy in an animal model of diabetes mellitus induced by a high-fat diet combined with a low-dose streptozotocin. In the in vitro experiments, SE treatment effectively suppressed the LPS-induced activation of key signaling pathways, including Akt, ERK1/2, p38 MAPK, and NF-κB, which are known to play pivotal roles in the inflammatory response. SE was also found to reduce oxidative stress and the production of inflammatory markers in the LPS-stimulated RAW264.7 cells. In the in vivo experiments, the administration of SE (500 mg/kg BW) and metformin (200 mg/kg BW) to high-fat diet/streptozotocin-induced diabetic rats effectively improved dyslipidemia, as evidenced by reductions in serum total cholesterol, LDL-cholesterol, and triglycerides compared to the untreated diabetic control group. Importantly, SE ameliorated the damage to the vascular endothelium and elastic fibers by downregulating the expression of proinflammatory cytokines and oxidative stress markers. Additionally, SE administration attenuated the upregulation of key markers associated with ER stress-mediated apoptotic pathways, with effects comparable to those observed in diabetic rats treated with the standard antidiabetic drug metformin. These findings suggest that SE possesses both anti-inflammatory and vascular protective properties, evident in both in vitro and in vivo studies.

摘要

我们之前的研究已表明桑约德大米乙醇提取物(SE)对脂质积累和胰岛素抵抗具有有益作用。然而,其对血管炎症的影响尚未得到探索。当前研究旨在调查SE在体外和体内模型中的抗炎作用,具体研究其对RAW264.7细胞中脂多糖(LPS)诱导的炎症的影响,并评估其在高脂饮食联合低剂量链脲佐菌素诱导的糖尿病动物模型中的疗效。在体外实验中,SE处理有效抑制了LPS诱导的关键信号通路的激活,包括Akt、ERK1/2、p38丝裂原活化蛋白激酶(MAPK)和核因子κB(NF-κB),这些信号通路在炎症反应中起关键作用。还发现SE可降低LPS刺激的RAW264.7细胞中的氧化应激和炎症标志物的产生。在体内实验中,给高脂饮食/链脲佐菌素诱导的糖尿病大鼠施用SE(500mg/kg体重)和二甲双胍(200mg/kg体重)可有效改善血脂异常,与未治疗的糖尿病对照组相比,血清总胆固醇、低密度脂蛋白胆固醇和甘油三酯降低证明了这一点。重要的是,SE通过下调促炎细胞因子和氧化应激标志物的表达,改善了血管内皮和弹性纤维的损伤。此外,SE给药减弱了与内质网应激介导的凋亡途径相关的关键标志物的上调,其效果与用标准抗糖尿病药物二甲双胍治疗的糖尿病大鼠中观察到的效果相当。这些发现表明,SE在体外和体内研究中均具有抗炎和血管保护特性。

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