研究内脂素对创伤性脑损伤（TBI）小鼠的神经功能保护作用及机制。

通过液压冲击方法建立C57BL/6小鼠液压冲击脑损伤模型，共48只，然后随机分为实验组A、实验组B、对照组，各16只。模型建立3 h后起，实验组A和实验组B分别给予腹腔注射内脂素15、30 μg/kg，1次/d，共7 d，对照组给予腹腔注射生理盐水。治疗开始前、开始治疗后第3、14、28天各组随机选取10只小鼠，比较实验组和对照组小鼠的神经功能缺损评分（NSS）；治疗结束后第2天，每组随机取3只小鼠全脑取材，比较TUNEL染色后阳性细胞差异；再随机取3只收集脑组织总蛋白，比较各组小鼠脑组织凋亡相关蛋白水平差异；剩余10只小鼠在治疗结束后第24~28天，比较Morris水迷宫小鼠逃逸潜伏期时间差异。

3组小鼠NSS评分在开始治疗后第3天时差异无统计学意义（P>0.05），但在第14、28天时，内脂素治疗组小鼠NSS评分低于对照组，差异均具有统计学意义（P<0.05）；3组小鼠在治疗结束后24、25 d时水迷宫潜伏逃逸期差异无统计学意义（P>0.05），但在第26、27、28天时，内脂素治疗组小鼠水迷宫潜伏逃逸期小于对照组，差异具有统计学意义（P<0.05）。内脂素治疗组小鼠脑切片中TUNEL阳性细胞数小于对照组，差异具有统计学意义（P<0.05），同时凋亡相关蛋白cleave Caspase-3、cleaved PARP的表达量也低于对照组，差异具有统计学意义（P<0.05）。

内脂素能够抑制小鼠TBI后病灶周围神经细胞的凋亡及降低凋亡相关蛋白的表达量，改善神经功能的修复。

To explore the neuroprotective effect and mechanism of visfatin in traumatic brain injury (TBI) mice model.

A total of 48 C57BL/6 mice with hydraulic shock brain injury model were established by means of hydraulic shock method, and then randomly divided into experimental group A, experimental group B and control group, 16 mice each. Three hours after the establishment of the model, experimental group A and experimental group B were given intraperitoneal injection of visfatin 15 and 30 μg/kg, respectively, once a day for 7 d, while the control group was given intraperitoneal injection of normal saline. Neurological severity scores (NSS) were compared before treatment, on day 3, day 14, and day 28 using 10 randomly selected mice. On the second day after the end of treatment, the whole brain of 3 mice in each group were randomly collected to compare the difference of positive cells after TUNEL staining, and then 3 mice were randomly collected from the brain tissue to compare the differences of apoptosis-related protein levels. The remaining 10 mice were compared with Morris water maze experiment from 24 to 28 d after treatment.

There was no statistical difference in NSS scores of 3 groups at day 3 (P>0.05), but at day 14 and 28, the NSS scores of the visfatin-treated group were lower than those of the control group, with significant differences (P<0.05). There was no statistically significant difference in the latent escape period of water maze in the 3 groups at the 24^th and 25^th day (P>0.05), but at the 26^th, 27^th and 28^th day, the latent escape period of water maze in the visfatin-treated group was smaller than that in the control group (P<0.05). The number of TUNEL positive cells in the brain sections of rats treated with lipoprotein was smaller than that of the control group (P<0.05), and the expression levels of apoptosis-related protein cleave caspase-3 and cleaved PARP were also lower than those of the control group (P<0.05).

Visfatin can inhibit the apoptosis of neural cells peripheral lesion and reduce the expression of apoptosis-related proteins after TBI in mice, improve the repair of neural function.