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TMP on cerebral infarct size after ischemia and ED1 IL-1β and TNF-α expression
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TMP on cerebral infarct size after ischemia and ED1 IL-1β and TNF-α expression
[Abstract] Objective To observe the TMP on cerebral infarct size after ischemia and ischemic brain tissue monoclonal antibody (ED1), interleukin-1β (IL-1β), tumor necrosis factor - @ (TNF- @) expression and to explore the mechanism of TMP. Methods 60 healthy adult SD male rats were randomly divided into sham operation group, model group and TMP large, medium, low dose group, copy the modified line tied to lack of law animal model of cerebral blood reperfusion. ligustrazine dose group were given 140 mg / kg intravenous TMP, in the dose group were given 120 mg / kg intravenous dose group were given 100 mg / kg intravenously. end of the experiment were killed large mice in each group obtained from the 6 rats in the brain tissue derived producer, TTC staining, formalin fixed, pathological image analysis system used to evaluate whether the reduction of infarct area of #8203;#8203;TMP; the other 6 groups rats brains were removed after production, by immunohistochemical staining ED1, IL-1β and TNF-@ in the positive. Results of the treatment group, TMP can reduce ischemia 90 min, 24 h reperfusion infarction area can also reduce the infarct region ED1, IL-1β and TNF-@’s immune expression. Conclusion TMP can reduce cerebral infarct size after reperfusion, the treatment effect may be related to inhibition of microglial activation and IL-1β, TNF-@ in the immunoreactive expression.
[Keywords:] TMP; cerebral ischemia-reperfusion injury; monoclonal antibody; interleukin-1β; tumor necrosis factor - @; rat
Abstract: Objective To investigate the effect of Tetramethyl Pyrazine (TMP) for treating cerebral infarct by observing infarct areas, and to research its function mechanism by observing the changes of the expressions of ED1, TNF-@ and IL-1β in the infarction region after focal cerebral ischemia reperfusion injury. Methods Sixty SD male rats in healthy condition were
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