| 大蒜素对感染性休克大鼠大脑海马CA1区保护作用的研究 |
| 投稿时间：2017-08-21 修订日期：2017-09-08 点此下载全文 |
| 引用本文：张昆.大蒜素对感染性休克大鼠大脑海马CA1区保护作用的研究[J].医学研究杂志,2018,47(12):181-186 |
| DOI：
10.11969/j.issn.1673-548X.2018.12.042 |
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| 中文摘要:目的 研究大蒜素对感染性休克大鼠脑组织海马CA1区的保护作用及相关作用机制。方法 采用尾静脉注射脂多糖（5mg/kg）的方法复制感染性休克大鼠模型，设模型组（生理盐水），大蒜素（0.3、3、6、12mg/kg）组，每组20只，另设正常对照组（生理盐水）20只，腹腔注射给药。24h后测定血清神经元特异性烯醇化酶（NSE）含量；测定脑组织海马区一氧化氮（NO）含量，抗氧化酶活性和丙二醛（MDA），测定炎性因子含量，HE染色观察脑组织海马CA1区病变、末端标记法（TUNEL）观察海马CA1区细胞凋亡，免疫组织化学法（IHC）检测脑组织Bcl-2、Bax蛋白表达。结果 6、12 mg/kg大蒜素能够显著降低感染性休克大鼠血清NSE含量和脑组织NO含量（P<0.05或P<0.01），改善抗氧化酶[超氧化物歧化酶（SOD）、过氧化氢酶（CAT）]活性并降低MDA含量（P<0.05或P<0.01），显著降低炎性细胞因子（TNF-α、IL-1β、IL-6）含量（P<0.05或P<0.01），明显改善海马CA1区病变和细胞凋亡状况，降低凋亡指数（AI）（P<0.01），上调Bcl-2表达并下调Bax表达、提高Bcl-2/Bax比值（P<0.05或P<0.01）。结论 大蒜素对感染性休克大鼠脑组织海马CA1区具有一定的保护作用，机制可能与抑制NSE、NO生成，抑制氧化应激损伤、炎性反应以及通过调节凋亡相关蛋白表达而抑制细胞凋亡有关。 |
| 中文关键词:大蒜素 感染性休克 脑组织 海马组织 凋亡 |
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| Protective Effect of Allicin on Hippocampal CA1 Region of Septic Shock Rats |
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| Abstract:Objective To study the protective effect of allicin on hippocampal CA1 region of septic shock rats and its related mechanism. Methods The rat model of septic shock was reproduced by tail vein injection of lipopolysaccharide (5mg/kg) and were randomly divided into model group, allicin (0.3, 3, 6, 12mg/kg) groups(n=20); and set normal control group(n=20). The drugs were administered by intraperitoneal injection. 24h later, the content of neuron-specific enolase (NSE) in serum and NO in brain were determined, the levels of inflammatory cytokines, antioxidant enzymes and malondialdehyde (MDA) in hippocampus tissue were measured. He morphological changes of neurons in hippocampus CA1 region were observed by HE Staining, the cell apoptosis were observed after TUNEL staining. The expression of Bcl-2 and Bax were exzamed by IHC. Results The content of neuron-specific enolase (NSE) in serum and NO in brain were significantly decreased in allicin (6, 12mg/kg) groups (P<0.05 or P<0.01), significantly improved in the activity of SOD, CAT and decreased in the content of MDA (P<0.05 or P<0.01), significantly decreased in the content of TNF-α, IL-1β, IL-6 (P<0.05 or P<0.01), significantly improved in the hippocampal CA1 neuronal pathological changes and apoptosis, significantly decreased in the apoptosis index (AI) (P<0.01), significantly up-regulated in the expression of Bcl-2 and down-regulated in the expression of Bax, increased in the Bcl-2/Bax ratio (P<0.05 or P<0.01). Conclusion Allicin has a certain protective effect on hippocampal CA1 region of septic shock rats, which perhaps related to its effects of depressing NSE, NO production, inhibiting oxidative stress injury, inflammatory response and apoptosis by modulating apoptosis-related protein expression. |
| keywords:Allicin Infection shock Brain tissue Hippocampus Apoptosis |
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