木槿花对大鼠脑缺血再灌注损伤的神经保护作用

Adjia Hamadjida , Saida Nkuketgnigni Njemguie , Rigobert Espoir Ayissi Mbomo , Stephen Nkengbang Foudjih , Véronique France Prisca Amayapa , Jean Pierre Kilekoung Mingoas , Fidèle Ntchapda
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引用次数: 0

摘要

背景木槿花(Hibiscus sabdariffa var. altissima)以其优质纤维而闻名,中医常用其利尿、利胆、镇痛、止咳和降压作用。此外,菊花还被用于治疗糖尿病、高血压、动脉粥样硬化和肥胖症。然而,目前还没有研究评估其对脑缺血的神经保护作用,这与以神经保护作用而闻名的沙巴叶品种不同。因此,本研究旨在探讨木槿提取物(HAS)对脑缺血再灌注(I/R)损伤过程中氧化应激和神经炎症的潜在疗效及其内在机制。方法通过大脑中动脉闭塞(MCAO)和再灌注建立雄性 Wistar 大鼠脑缺血模型。将大鼠随机分为假组、IR 组、IR + HSA100 组、IR + HSA200 组、IR + HSA400 组和 IR + Eda 组,连续治疗 14 天。进行神经功能缺损评分和量筒测试以评估神经功能损伤。通过测量丙二醛(MDA)水平确定氧化应激,并测量还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)等抗氧化标志物以评估抗氧化活性。此外,还测定了肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)等炎症细胞因子的水平。HSA 还降低了脑组织中 MDA 的水平,提高了 GSH、SOD 和 CAT 的抗氧化活性。此外,HSA 还能降低血清中促炎细胞因子 TNF-α、IL-1β 和 IL-6 的表达。因此,HSA 可作为脑缺血损伤的一种潜在治疗选择。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Neuroprotective effects of Hibiscus sabdariffa var. altissima on cerebral ischemia‒Reperfusion injury in rats

Neuroprotective effects of Hibiscus sabdariffa var. altissima on cerebral ischemia‒Reperfusion injury in rats

Background

Hibiscus sabdariffa var. altissima, which is known for its high-quality fiber, is commonly used in Traditional Chinese Medicine (TCM) for its diuretic, choleretic, analgesic, antitussive, and hypotensive effects. Furthermore, the flowers have been used to treat diabetes, hypertension, atherosclerosis, and obesity. However, there are no studies assessing its neuroprotective effects on cerebral ischemia, unlike the sabdariffa variety known for its neuroprotective effects. Therefore, this study was aimed to investigate the potential efficacy of Hibiscus sabdariffa var. altissima extract (HAS) and its underlying mechanism on oxidative stress and neuroinflammation during cerebral ischemia-reperfusion (I/R) injury.

Methods

A model of cerebral ischemia was established in male Wistar rats through middle cerebral artery occlusion (MCAO) and reperfusion. Rats were randomly divided into the sham, IR, IR + HSA100, IR + HSA200, IR + HSA400 and IR + Eda groups and were treated for 14 consecutive days. The neurological deficit score and the cylinder test were performed to assess neurological impairment. Oxidative stress was determined by measuring the levels of malondialdehyde (MDA) and antioxidant markers such as reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were measured to evaluate antioxidant activities. In addition, the levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), were also determined.

Results

Our results demonstrated that HSA significantly ameliorated neurological impairment and reduced the volume of brain infarct. HSA also decreased the levels of MDA and enhanced the antioxidant activities of GSH, SOD and CAT in brain tissues. Furthermore, HSA decreased the expression of the proinflammatory cytokines TNF-α, IL-1β and IL-6 in the serum.

Conclusion

These findings demonstrated that HSA exhibited a potential neuroprotective effect against cerebral I/R injury, possibly by improving oxidative stress and attenuating inflammatory responses. Therefore, HSA could be used as a potential therapeutic option for cerebral ischemic injuries.

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