摘要:目的:動態觀察大鼠腦出血后血腫周圍組織補體激活與細胞凋亡的規律。方法:用膠原酶注入到大鼠尾狀核的方法制作腦出血模型。將大鼠分為腦出血、假手術組、正常組3組。采用蘇木素伊紅(HE) 染色、免疫組織化學染色及原位末端脫氧核苷酸轉移酶介導的dUTP 缺口末端標記法(TUNEL)分別觀察各組在腦出血后第6 h、12 h、24 h、48 h、72 h、5 d、7 d時血腫周圍補體C3、促凋亡基因(Bax)、抑凋亡基因(Bclxl)及TUNEL的表達。結果補體C3的表達峰值在24~48 h;TUNEL、Bax蛋白表達術后12h增加,48~72 h達高峰,而Bclxl蛋白表達高峰在48h。結論:大鼠腦出血后血腫周圍組織補體C3的表達增加與細胞凋亡的演變趨勢一致,C3與凋亡有相關。Abstract: Objective: To study the complement activation and apoptosis regular genes changes in the tissues of the perihematoma of intracerebral hemorrhage (ICH) in rats. Methods: Intracerebral hemorrhage was induced in rats by injection of bacterial collagenase into the caudate nucleus. Histopathological changes were studied in 6 h,12 h, 24 h, 2 d, 3 d, 5 d, 7 d after the injection. The immunohistochemistry and TUNEL analysis were performed. The expression of complement factor C3, the TUNELpositive cells, the proapoptotic gene expression (Bax) and the antiapoptotic gene (Bclxl) were examined. Results: The expression of C3 increased to its maximum between 2448 h. The TUNELpositive cells and Bax protein expression increased gradually and reached the peak level between 4872 h. The Bclxl protein reached the peak level at 48 h. The correlation analysis showed that the quantity of C3 was positively related to that of the TUNELpositive cells, but the bax protein was not related to Bclxl protein. Conclusion: The expression of complement factor C3 may contributes to the nerve injury after cerebral hemorrhage and relate to the apotosis in the tissues surrounding the hametoma in rats.
摘要:目的:探討卡配因抑制劑3（MDL28170）對新生大鼠缺氧缺血性腦損傷(HIBD)神經細胞凋亡的影響。方法:建立新生SD大鼠HIBD模型,治療組于缺養缺血后即刻、2 h、4 h腹腔內注射MDL28170,對照組及手術組同時予生理鹽水。缺氧缺血后24 h用免疫組化方法觀察大腦皮質及海馬CA1區Caspase3 蛋白表達、TUNEL法檢測細胞凋亡,觀察組織病理改變并計算海馬神經元死亡數,透射電鏡觀察細胞超微結構。結果:缺氧缺血后24 h缺血側大腦皮質及海馬CA1區Caspase3和TUNEL陽性細胞數較對照組明顯增加,透射電鏡證實有凋亡細胞;MDL28170可減少陽性細胞數量,抑制神經元死亡,差異有顯著性(Plt;0.05)。結論:MDL28170可通過抑制神經凋亡而對新生大鼠HIBD具有一定保護作用。Abstract: Objective: To investigate the effect of (Calpain inhibitor3) MDL28170 on neural apoptosis in a neonatal model of hypoxicischemic brain damage (HIBD). Methods: A neonatal model of HIBD was established, 7dayold SD rats were divided into three groups. The treatment group received MDL28170(ip) at 0 h,2 h,4 h after HI, whereas the other two groups were administered normal saline simultaneously. The expression of caspase3 (by immunohistochemistry), neural apoptosis (by TUNEL) in cortex and hippocampus ipsilateral to the insult were observed 24 h after HI; hippocampal CA1 neural loss and electromicroscopic changes were assessed at the same time. Results: Apoptotic body was observed by electromicroscopy. Caspase3 positive cells and apoptotic cells increased significantly in the ipsilateral cortex and hippocampal CA1 region compared to the control, and MDL28170 reduced the number of positive cells, attenuated CA1 neural loss with significance (Plt;0.05). Conclusion: It is suggested that MDL28170 may protect the brain of neonatal rats after HIBD by suppressing neural apoptosis.
