体育学刊
體育學刊
체육학간
Journal of Physical Education
2014年
5期
139~144
,共null页
赵广高 苏全生 周石 苏利强 张玮
趙廣高 囌全生 週石 囌利彊 張瑋
조엄고 소전생 주석 소리강 장위
运动生理学 Th1 Th2平衡 Janus激酶-2 信号传导与转录激活因子-4 白细胞介素-12 γ-干扰素 白细胞介素-4
運動生理學 Th1 Th2平衡 Janus激酶-2 信號傳導與轉錄激活因子-4 白細胞介素-12 γ-榦擾素 白細胞介素-4
운동생이학 Th1 Th2평형 Janus격매-2 신호전도여전록격활인자-4 백세포개소-12 γ-간우소 백세포개소-4
sports physiology;Th1/Th2 balance; JAK2; STAT4; IL-12; IFN-γ; IL-4
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。
通過遊泳訓練誘髮大鼠Th1/Th2失衡,觀察和分析JAK2/STAT4通路及其上遊因子在該失衡髮展過程中的變化規律,探討大運動量訓練導緻Th1/Th2失衡的分子機製。將清潔級16週齡雄性SD大鼠隨機分為安靜對照組(C組)、遊泳訓練組(T組),每組根據取材時間不同又隨機分為24 h組與7 d組。訓練採用4週遞增負荷遊泳訓練方法。Western Blotting法測定心髒血淋巴細胞pJAK2、pSTAT4、JAK2、STAT4的蛋白錶達,ELISA法檢測心髒血血漿IFN-γ、IL-4、IL-12值。結果髮現:(1)T組大鼠血漿IFN-γ、IFN-γ/IL-4與IL-12(P〈0.01)水平均顯著低于C組(P〈0.01)、(P〈0.05)。C組與T組大鼠血漿IL-12與IFN-γ的質量濃度顯著相關(P〈0.01)。(2)T組大鼠血淋巴細胞pJAK2、pSTAT4蛋白錶達均顯著低于C組(P〈0.05)、(P〈0.01)。結果說明4週遞增負荷訓練可能通過減少IL-12的分泌,抑製JAK2/STAT4信號通路中關鍵因子JAK2、STAT4的燐痠化過程,降低Th1類細胞因子IFN-γ的閤成,誘髮Th1/Th2失衡。
통과유영훈련유발대서Th1/Th2실형,관찰화분석JAK2/STAT4통로급기상유인자재해실형발전과정중적변화규률,탐토대운동량훈련도치Th1/Th2실형적분자궤제。장청길급16주령웅성SD대서수궤분위안정대조조(C조)、유영훈련조(T조),매조근거취재시간불동우수궤분위24 h조여7 d조。훈련채용4주체증부하유영훈련방법。Western Blotting법측정심장혈림파세포pJAK2、pSTAT4、JAK2、STAT4적단백표체,ELISA법검측심장혈혈장IFN-γ、IL-4、IL-12치。결과발현:(1)T조대서혈장IFN-γ、IFN-γ/IL-4여IL-12(P〈0.01)수평균현저저우C조(P〈0.01)、(P〈0.05)。C조여T조대서혈장IL-12여IFN-γ적질량농도현저상관(P〈0.01)。(2)T조대서혈림파세포pJAK2、pSTAT4단백표체균현저저우C조(P〈0.05)、(P〈0.01)。결과설명4주체증부하훈련가능통과감소IL-12적분비,억제JAK2/STAT4신호통로중관건인자JAK2、STAT4적린산화과정,강저Th1류세포인자IFN-γ적합성,유발Th1/Th2실형。
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.