Chinese Journal of Tissue Engineering Research ›› 2025, Vol. 29 ›› Issue (30): 6474-6481.doi: 10.12307/2025.781
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Zhang Songjiang, Li Longyang, Zhou Chunguang, Gao Jianfeng
Received:
2024-09-09
Accepted:
2024-11-02
Online:
2025-10-28
Published:
2025-03-28
Contact:
Gao Jianfeng, MD, Professor, Master’s supervisor, Medical College of Henan University of Chinese Medicine, Zhengzhou 450046, Henan Province, China
About author:
Zhang Songjiang, MD, Professor, Master’s supervisor, Medical College of Henan University of Chinese Medicine, Zhengzhou 450046, Henan Province, China
Supported by:
CLC Number:
Zhang Songjiang, Li Longyang, Zhou Chunguang, Gao Jianfeng. Central anti-inflammatory effect and mechanism of tea polyphenols in exercise fatigue model mice[J]. Chinese Journal of Tissue Engineering Research, 2025, 29(30): 6474-6481.
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2.1 实验动物数量分析 实验过程无小鼠脱失,3组小鼠共24只进入结果分析。 2.2 小鼠力竭游泳时间 与疲劳模型组相比,茶多酚组小鼠力竭游泳时间显著延长(P < 0.05),见图1。结果说明茶多酚有抗疲劳和增强小鼠运动能力的作用。 2.3 小鼠脑组织苏木精-伊红染色结果 与安静对照组相比,疲劳模型组和茶多酚组海马组织致密性没有明显变化,细胞排列整齐,紫蓝色的细胞核清晰可见,胞核与胞浆对比鲜明,形态结构未见明显异常,见图2。 2.4 小鼠脑组织肿瘤坏死因子α、白细胞介素1β和白细胞介素10蛋白表达 免疫印迹检测结果显示,与安静对照组相比,疲劳模型组小鼠脑组织肿瘤坏死因子α和白细胞介素1β表达均明显增加(P < 0.01),白细胞介素10表达明显减少(P < 0.01);与疲劳模型组相比,茶多酚组小鼠脑组织肿瘤坏死因子α和白细胞介素1β表达明显减少(P < 0.05,P < 0.01),白细胞介素10表达明显增加(P < 0.01);与安静对照组相比,茶多酚组小鼠脑组织肿瘤坏死因子α和白细胞介素1β表达均明显增加(P < 0.05),白细胞介素10表达明显减少(P < 0.05),见图3。结果说明运动疲劳后神经中枢有炎症反应,而茶多酚有缓解炎症的作用,但是茶多酚对运动疲劳所致的中枢炎症的缓解作用尚未达到安静组水平。 2.5 小鼠脑组织诱导型一氧化氮合酶和精氨酸酶1蛋白表达 不同的小胶质细胞的亚型发挥不同的生物学效应。采用免疫印迹检测各组小鼠脑组织M1型(标志蛋白:诱导型一氧化氮合酶) 和M2型 ( 标志蛋白:精氨酸酶1 ) 小胶质细胞标志蛋白水平。结果显示,与安静对照组相比,疲劳模型组小鼠脑组织诱导型一氧化氮合酶表达明显增加(P < 0.01),精氨酸酶1表达明显减少(P < 0.01);与疲劳模型组相比,茶多酚组小鼠脑组织诱导型一氧化氮合酶表达明显降低(P < 0.01),而精氨酸酶1表达明显增加 (P < 0.01);与安静对照组相比,茶多酚组小鼠脑组织诱导型一氧化氮合酶表达明显增加(P < 0.05),精氨酸酶1表达明显减少(P < 0.05),见图4。结果说明,茶多酚抑制小胶质细胞诱导型一氧化氮合酶的表达,促进精氨酸酶1的表达,对激活的小胶质细胞由M1型向M2型转化有积极的促进作用,但是茶多酚对运动疲劳所致小胶质细胞的转化作用还没有恢复到安静组水平。 2.6 小鼠脑组织p-STAT3和核因子κB p65蛋白表达 免疫印迹检测结果显示,与安静对照组相比,疲劳模型组小鼠脑组织p-STAT3和核因子κB p65表达明显增加(P < 0.01);与疲劳模型组相比,茶多酚组小鼠脑组织p-STAT3和核因子κB p65表达明显降低(P < 0.01,P < 0.05);与安静对照组相比,茶多酚组小鼠脑组织核因子κB p65表达明显增加(P < 0.05),见图5。结果说明,小鼠运动疲劳的中枢炎症反应可能是通过激活STAT3/核因子κB p65信号通路实现的,茶多酚对脑组织炎症反应缓解作用是通过抑制STAT3/核因子κB p65信号通路实现的,但是茶多酚对运动疲劳情况下的κB p65信号通路的抑制作用还没有恢复到安静组水平。 2.7 小鼠脑组织STAT3 mRNA和核因子κB p65 mRNA水平 实时荧光定量聚合酶链式反应检测结果显示,与安静对照组相比,疲劳模型组小鼠脑组织STAT3 mRNA和核因子κB P65 mRNA水平明显升高(P < 0.01);与疲劳模型组相比,茶多酚组小鼠脑组织STAT3 mRNA和核因子κB p65 mRNA水平明显降低(P < 0.05)。与安静对照组相比,茶多酚组小鼠脑组织STAT3 mRNA和核因子κB p65水平明显升高(P < 0.05),见图6。结果说明,不论是运动疲劳和茶多酚的干预,STAT3/核因子κB p65信号分子水平从基因转录水平已经有了改变,而且这个改变和蛋白的表达水平是一致的。 2.8 血浆白细胞介素1β、白细胞介素10和肿瘤坏死因子α的酶联免疫吸附检测结果 见图7。酶联免疫吸附检测结果显示,与安静对照组相比,疲劳模型组小鼠血浆肿瘤坏死因子α和白细胞介素1β质量浓度明显增加(P < 0.01),白细胞介素10质量浓度明显降低(P < 0.01);与疲劳模型组相比,茶多酚组小鼠血浆肿瘤坏死因子α和"
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