通过游泳训练诱发大鼠Th1/Th2失衡，观察和分析JAK2/STAT4通路及其上游因子在该失衡发展过程中的变化规律，探讨大运动量训练导致Th1/Th2失衡的分子机制。将清洁级16周龄雄性SD大鼠随机分为安静对照组(C组)、游泳训练组(T组)，每组根据取材时间不同又随机分为24 h组与7 d组。训练采用4周递增负荷游泳训练方法。Western Blotting法测定心脏血淋巴细胞pJAK2、pSTAT4、JAK2、STAT4的蛋白表达，ELISA法检测心脏血血浆IFN-γ、IL-4、IL-12值。结果发现：(1)T组大鼠血浆IFN-γ、IFN-γ/IL-4与IL-12(P<0.01)水平均显著低于C组(P<0.01)、(P<0.05)。C组与T组大鼠血浆IL-12与IFN-γ的质量浓度显著相关(P<0.01)。(2)T组大鼠血淋巴细胞pJAK2、pSTAT4蛋白表达均显著低于C组(P<0.05)、(P<0.01)。结果说明4周递增负荷训练可能通过减少IL-12的分泌，抑制JAK2/STAT4信号通路中关键因子JAK2、STAT4的磷酸化过程，降低Th1类细胞因子IFN-γ的合成，诱发Th1/Th2失衡。%By means of swimming training, the authors induced rat’s Th1/Th2 imbalance, observed and analyzed the patterns of changing of JAK2/STAT4 pathways and their upstream cytokines in the process of development of such an imbalance, so as to probe into the molecular mechanism of intensive training inducing the Th1/Th2 imbalance. The authors randomly divided 16-week old male SD rats graded clean into a calm control group (group C) and a swimming training group (group T), then randomly divided each of these groups into a 24h group and a 7d group according to different sampling times, carried out the training by using the 4-week load progressively increased swimming training method, measured the protein expressions of pJAK2, pSTAT4, JAK2 and STAT4 in cardiac blood lymphocytes by using the western blotting method, measured the contents of IFN-γ, IL-4 and IL-12 in cardiac blood plasma by using the ELISA method, and revealed the following findings: 1) the levels of IFN-γ, IFN-γ/IL-4 and IL-12 in blood plasma of the rats in group T were all significantly lowered that those of the rats in group C (P<0.01,P<0.05,P<0.01); the contents of IL-12 and IFN-γ in blood plasma of the rats in groups C and T were sig- nificantly correlative (P<0.01); 2) the protein expressions of pJAK2 and pSTAT4 in blood lymphocytes of the rats in group T were all significantly lowered that those of the rats in group C (P<0.05,P<0.01). The said findings indicate that the 4-week load progressively increased training may induce the Th1/Th2 imbalance by reducing the secretion of IL-12, suppressing the process of phosphorylation of key cytokines JAK2 and STAT4 in JAK2/STAT4 signaling pathways, and reducing the synthesis of type Th1 cytokine IFN-γ.
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