Anti-inflammation effects of picroside 2 in cerebral ischemic injury rats.
Anti-inflammation effects of picroside 2 in cerebral ischemic injury rats.
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DOI：
10.1186/1744-9081-6-43
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发表时间：
2010-07-09
期刊：
影响因子：
--
通讯作者：
Du F
中科院分区：
文献类型：
--
作者：
Guo Y;Xu X;Li Q;Li Z;Du F
兴奋性氨基酸毒性、氧化应激、细胞内钙超载以及炎症和细胞凋亡参与了脑缺血再灌注损伤后的病理过程。Picrodide 2在脑缺血再灌注损伤中可抑制神经细胞凋亡，发挥抗氧化和抗炎作用，但其确切机制尚不十分清楚。本研究旨在探讨胡黄连苷2在大鼠脑缺血再灌注损伤中的抗炎作用机制。采用线栓法建立90只成年健康雌性Wistar大鼠大脑中动脉闭塞再灌注模型。胡黄连苷2和丹参素A钠分别以10 mg/kg剂量尾静脉注射治疗。采用Bederson试验评价神经行为功能，氯化四氮唑（TTC）染色观察脑梗死体积。采用原位末端脱氧核苷酸转移酶介导的缺口末端标记法（TUNEL）检测凋亡细胞。免疫组化法检测Toll样受体4（TLR 4）、核转录因子κB（NFκB）和肿瘤坏死因子α（TNFα）的表达。采用酶联免疫吸附法（ELISA）测定脑组织中TLR 4、NFκB和TNFα的含量。脑缺血再灌注后，大鼠出现神经行为功能障碍和缺血侧脑梗死。缺血对照组脑组织中凋亡细胞数、TLR 4、NFκB和TNFα的表达及含量均较假手术组明显增加（P < 0.01）。胡黄连苷2组和丹参素A钠组神经行为学评分、脑梗死体积、脑组织中凋亡细胞数、TLR 4、NFκB和TNFα的表达和浓度均明显低于缺血对照组（P < 0.01）。治疗组与对照组比较，上述指标差异无统计学意义（P > 0.05）。胡黄连苷2通过下调TLR 4、NFκB和TNFα的表达，抑制脑缺血再灌注损伤诱导的细胞凋亡和炎症反应，改善大鼠神经行为功能。
Excitatory amino acid toxicity, oxidative stress, intracellular calcium overload, as well as inflammation and apoptosis are involved in the pathological process after cerebral ischemic reperfusion injury. Picrodide 2 could inhibit neuronal apoptosis and play anti-oxidant and anti-inflammation role in cerebral ischemia/reperfusion injuries, but the exact mechanism is not very clear. This study aims to explore the anti-inflammation mechanism of picroside 2 in cerebral ischemic reperfusion injury in rats. The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in 90 adult healthy female Wistar rats. Picroside 2 and salvianic acid A sodium were respectively injected from tail vein at the dosage of 10 mg/kg for treatment. The neurobehavioral function was evaluated with Bederson's test and the cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The apoptotic cells were counted by in situ terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The immunohistochemistry stain was used to determine the expressions of toll-like receptor 4 (TLR4), nuclear transcription factor κB (NFκB) and tumor necrosis factor α (TNFα). The concentrations of TLR4, NFκB and TNFα in brain tissue were determined by enzyme linked immunosorbent assay (ELISA). After cerebral ischemic reperfusion, the rats showed neurobehavioral function deficit and cerebral infarction in the ischemic hemisphere. The number of apoptotic cells, the expressions and the concentrations in brain tissue of TLR4, NFκB and TNFα in ischemia control group increased significantly than those in the sham operative group (P < 0.01). Compared with the ischemia control group, the neurobehavioral scores, the infarction volumes, the apoptotic cells, the expressions and concentrations in brain tissue of TLR4, NFκB and TNFα were obviously decreased both in the picroside 2 and salvianic acid A sodium groups (P < 0.01). There was no statistical difference between the two treatment groups in above indexes (P > 0.05). Picroside 2 could down-regulate the expressions of TLR4, NFκB and TNFα to inhibit apoptosis and inflammation induced by cerebral ischemic reperfusion injury and improve the neurobehavioral function of rats.
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DOI：
10.3969/j.issn.0529-1356.2010.01.002
发表时间：
2010-02-01
期刊：
Jiepou Xuebao
影响因子：
--
作者：
Li Zhen;Li Qin;Luan Li-ju
通讯作者：
Luan Li-ju
玄黄连乙醇提取物通过抗炎作用预防实验性糖尿病肾损伤
影响因子：
4
作者：
He, Li Juan;Liang, Min;Zhang, Xun
通讯作者：
Zhang, Xun
影响因子：
8.3
作者：
BEDERSON, JB;PITTS, LH;BARTKOWSKI, H
通讯作者：
BARTKOWSKI, H
影响因子：
5.3
作者：
Kaushal, Vikas;Schlichter, Lyanne C.
通讯作者：
Schlichter, Lyanne C.
影响因子：
6.1
作者：
Webster CM;Kelly S;Koike MA;Chock VY;Giffard RG;Yenari MA
通讯作者：
Yenari MA