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(jīng)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(yǎng)缺血后即刻、2 h、4 h腹腔內(nèi)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(zhì)及海馬CA1區(qū)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(jīng)元死亡數(shù),透射電鏡觀察細胞超微結(jié)構(gòu)。結(jié)果:缺氧缺血后24 h缺血側(cè)大腦皮質(zhì)及海馬CA1區(qū)Caspase3和TUNEL陽性細胞數(shù)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(shù)量,抑制神經(jīng)元死亡,差異有顯著性(Plt;0.05)。結(jié)論:MDL28170可通過抑制神經(jīng)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.
目的 探討嬰兒急性白血?。↖AL）的臨床與實驗室檢查特征。 方法 對1999年12月－2011年6月收治的15例嬰兒急性白血病的臨床資料進行總結(jié)與分析。 結(jié)果 其中急性淋巴細胞白血病（ALL）6例，急性髓系白血病（AML）8例，分類不明1例，其中以M4（4例）、M5（3例）為主。臨床表現(xiàn)多樣，髓外浸潤明顯。1例細胞形態(tài)學與免疫分型有差異，1例合并染色體異常。放棄治療者11例，死亡2例，正規(guī)治療的2例于誘導緩解后獲完全緩解。 結(jié)論 IAL預后差，需完善相關檢查并不斷總結(jié)臨床資料以提高IAL治愈率。