有氧运动激活肥胖大鼠前额叶PPARγ-PI3K-Akt通路并促进神经可塑性相关蛋白表达

采用高脂饮食建立肥胖大鼠模型，使用Western印迹检测大鼠前额叶PPARγ- PI3K-Akt通路及神经可塑性相关蛋白质表达，明确高脂饮食诱导肥胖后对大鼠前额叶神经可塑性影响及观察有氧运动的调节作用。结果表明，与对照组（CS）相比，高脂饮食肥胖大鼠（OS）前额叶过氧化物酶体增殖剂激活受体（PPARγ）（0.46±0.07 vs. 0.81±0.09, P<0.01）、p-PI3K/PI3K（0.21±0.04 vs. 0.36±0.03, P<0.05）与p-Akt/Akt（0.22±0.04 vs. 0.33±0.05, P<0.05）比值、脑源性神经生长因子（BDNF）（0.71±0.08 vs. 1.06±0.10, P<0.01）及突触素（SYN）（0.18±0.03 vs. 0.36±0.03, P<0.01）表达均显著下降；凋亡相关蛋白质胱天蛋白酶9（0.37±0.05 vs. 0.18±0.01, P<0.01）表达及Bax/Bcl-2（2.95±0.73 vs. 0.94±0.18, P<0.01）比值显著升高。有氧运动后，与安静肥胖组(OS)相比，肥胖运动组(OE)大鼠前额叶PPARγ（0.65±0.11 vs. 0.46±0.07, P<0.05）、p-PI3K/PI3K（0.33±0.06 vs. 0.21±1.04, P<0.05）与p-Akt/Akt（0.31±0.05 vs. 0.22±0.04, P<0.05）比值显著上调；胱天蛋白酶9（0.22±0.04 vs. 0.37±0.05, P<0.05）及Bax/Bcl-2（1.74±0.43 vs. 2.95±0.43 P<0.05）比值显著下调。但是，BDNF（0.92±0.16 vs. 0.71±0.08）及SYN（0.30±0.04 vs. 0.18±0.03）表达无显著差异。结果提示，高脂饮食可导致肥胖大鼠前额叶神经可塑性相关蛋白质表达下降，其机制可能与神经细胞凋亡的发生有关。有氧运动可通过激活PPAR-γ-PI3K-Akt通路途径抑制细胞凋亡的发生，促进神经可塑性相关蛋白质的表达。

Aerobic Exercise Activates the PPARγ-PI3K-Akt Pathway and Promotes Neuroplasticity Related Gene Expression in the Obese Rat Prefrontal Cortex

In the study, we established an obese rat model by feeding rats with a high-fat diet. We aim to determine the effect on the neuroplasticity of the prefrontal cortex in high fat diet-inducedobesity and to observe the regulation of aerobic exercise. The production of PPARγ-PI3K-Akt pathway protein components and neural plasticity-related proteins in the rat prefrontal cortex was detected by Western blotting. The results showed that compared with the control group（CS），the levels of PPARγ（0.46±0.07 vs. 0.81±0.09, P<0.01）, p-PI3K / PI3K（0.21±0.04 vs. 0.36±0.03, P<0.05）, p-Akt / Akt（0.22±0.04 vs. 0.33±0.05, P<0.05）, BDNF（0.71±0.08 vs. 1.06±0.10, P<0.01）and SYN（0.18±0.03 vs. 0.36±0.03, P<0.01）in the prefrontal cortex of the obesity sedentary group (OS) significantly decreased, while the levels of caspase 9（0.37±0.05 vs. 0.18±0.01, P<0.01）and Bax / Bcl-2（2.95±0.73 vs. 0.94±0.18, P<0.01）significantly increased. Compared with OS, the expressions of PPARγ, p-PI3K / PI3K（0.33±0.06 vs. 0.21±0.04, P<0.05）and p-Akt / Akt（0.31±0.05 vs. 0.22±0.04, P<0.05）in the obesity with aerobic exercise (OE) group significantly increased and the levels of caspase 9（0.22±0.04 vs. 0.37±0.05, P<0.05）and Bax / Bcl-2（1.74±0.43 vs. 2.95±0.43,P<0.05）significantly decreased after aerobic exercise. However, the levels of BDNF（0.92±0.16 vs. 0.71±0.08）and SYN（0.30±0.04 vs. 0.18±0.03）were not significant different compared with OS and OE groups. The results suggest that high-fat diets may decrease the expression of plasticity-related genes in the prefrontal cortex of OS, which may be related to the occurrence of neuronal apoptosis. On the contrary, aerobic exercise may promote the expression of neuroplasticity-related genes through activation of the PPARγ-PI3K-Akt pathway to inhibit apoptosis.