Generation of a fusion protein between trastuzumab and unique long-16 binding protein 2 to stimulating immune cells to kill the breast carcinoma in vitro

Abstract

Objective To research the protective effect of lidocaine on mitochondria damage caused by isoflurane in hippocampus of old rats. Methods The 18-month-old Fisher 344 rats were divided into 3 groups (6 rats per group): control group, 1.2% isoflurane group and 1.2% isoflurane + lidocaine group. The apoptosis was examined through TdT-mediated dUTP nick end labeling (TUNEL), the expression of cysteinyl aspartate-specific protease (Caspase)-3 and B cell lymphoma/leukemia-2 associated X protein (bax)/B cell lymphoma/leukemia-2 (bcl-2) was detected by Western blotting, and mitochondria morphological characteristics were observed through electron microscope. The activity of mitochondrial respiratory chain and the mitochondrial membrane potential were tested. Results By comparison with control group, isoflurane could not only increase apoptosis rate, but also increase the expression of Caspase-3 [(0.11±0.04)% vs. (0.30±0.09)%] and bax/bcl-2 [(0.6±0.2)% vs. (2.4±0.9)%]. However lidocaine reduced the expression of Caspase-3 and bax/bcl-2. As compared with control group, isoflurane depressed the activity of mitochondrial respiratory chain and the mitochondrial membrane potential [(14.1±4.8)% vs. (85.9±3.5)%]. After adding lidocaine, the activity and potential were elevated to (52.5±5.9)%. Conclusion Lidocaine could relieve the neurotoxicity of isoflurane though reducing mitochondria damage in hippocampus of old rats. Key words: Lidocaine; Isoflurane; Mitochondrion; Hippocampus neurons; Apoptosis