中文摘要：

目的：研究14—3—3γ在烧伤及脂多糖（LPS）引起的心肌损伤中的保护作用。方法：体内实验建立大鼠烧伤及LPS损伤模型，检测3、6、12、24h各时点心功能及心肌细胞14—3—3γ蛋白表达水平的改变；体外实验采用新生大鼠心肌细胞，构建pFLAG-14-3-3γ质粒，于LPS损伤前24h转染至心肌细胞，实验结束后检测培养液中乳酸脱氢酶（LDH）活性，MTT法测定细胞存活率，流式细胞术检测细胞凋亡，线粒体肿胀实验检测线粒体通透性转换孔（mPTP）开放。结果：烧伤及LPS损伤模型大鼠心电图sT段均有明显改变，心肌细胞14—3—3γ蛋白表达水平均显著升高。转染了pFLAG—14—3—3γ质粒的心肌细胞能明显对抗随后的LPS损伤，与未转染组比较，14—3—3γ能明显提高细胞存活率，降低LDH活性，减少细胞凋亡，抑制mPTP的开放。结论：14—3—3γ可能通过抑制mFrP的开放对烧伤及LPS所致的心肌损伤起保护作用。

英文摘要：

To study the protective role of 14 -3 -3γ in burn or LPS- induced myocardial injury. METHODS： The ray/model of burn or LPS- induced injury was established. The heart functions and 14 -3 -3γ protein expression were detected 3 h,~fi~, 12 h and 24 h after treatment. Primary neonatal rat eardiomyocytes were used in vitro.pFLAG - 14 - 3 γ ted and transfected into the cardiomyocytes 24 h before LPS - induced injury.The injury in the cardi~omyocytes was ev~u~ed by measuring the cell viability and the level of lactate dehydrogenase （LDH）. Apoptosis of cardiomyocytes was detec~ by flow cytometry. Opening of mitochondrial permeability transition pore （mPTP） was also determined by Ca2 ＋ - induced s~lling of isolated myocardial mitochondria. RESULTS： The expression of 14 -3 -3-γwas elevated following the burn or LPS -Induced myocardial injury/n v/to. In vitro, transfection with pFLAG-14 -3 -3T plasmid in to the cardiomyocytes signiflcantly protected against LPS -induced injury. Compared with the car- diomyocytes without transfection with pFLAG - 14 - 3 - 3,/plasmid, higher cell viability rate and lower LDH release, cell ap- optosis and opening were observed in the cardiomyocytes transfected with pFLAG - 14 - 3 - 3γ plasmid. CONCLU- SION： The 14 -3 -3γ protein protects the heart against burn or LIS -induced injury by inhibiting the mPTP opening.