Exercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10.

Exercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10.
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DOI:
10.3389/fphys.2015.00124
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发表时间:
2015
影响因子:
4
通讯作者:
Mishra PK
Mishra PK
中科院分区:
医学2区
文献类型:
--
作者:
Kesherwani V;Chavali V;Hackfort BT;Tyagi SC;Mishra PK

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越来越多的证据表明,久坐不动的生活方式和高脂肪饮食(HFD)会导致心肌病。适度运动可改善心功能不全,但其分子机制尚不清楚。由于促炎细胞因子如肿瘤坏死因子-α(TNF-α)的诱导和抗炎细胞因子如白细胞介素10(IL-10)的减弱导致的炎症增加导致肥胖和糖尿病患者的心功能障碍。我们假设运动训练通过上调IL-10和下调TNF-α减轻肥胖和炎症,从而改善HFD诱导的心功能不全。为了检验这一假设,用HFD喂养8周龄雌性C57 BL/6 J小鼠并进行锻炼(游泳1小时/天,持续5天/周,持续8周)。四个治疗组:分析正常饮食(ND)、HFD、HFD +运动(HFD + Ex)和ND + Ex的平均体重、血糖水平、TNF-α、IL-10、Masson三色法测定的心脏纤维化和超声心动图测定的心功能不全。平均体重在HFD中增加,但在HFD + Ex中相对较少。HFD组TNF-α水平升高,IL-10水平下调,HFD + Ex组TNF-α水平升高,IL-10水平下调。心脏纤维化在HFD中增加,并且在HFD + Ex组中通过运动而减弱。射血分数和短轴缩短率在HFD中降低,但在HFD + Ex中相对增加。ND组与ND + Ex组除IL-10水平在运动后升高外,其余指标无显著性差异。基于这些结果,我们得出结论,运动通过减少肥胖、诱导IL-10和降低TNF-α来减轻HFD诱导的心肌病。
Increasing evidence suggests that a sedentary lifestyle and a high fat diet (HFD) leads to cardiomyopathy. Moderate exercise ameliorates cardiac dysfunction, however underlying molecular mechanisms are poorly understood. Increased inflammation due to induction of pro-inflammatory cytokine such as tumor necrosis factor-alpha (TNF-α) and attenuation of anti-inflammatory cytokine such as interleukin 10 (IL-10) contributes to cardiac dysfunction in obese and diabetics. We hypothesized that exercise training ameliorates HFD- induced cardiac dysfunction by mitigating obesity and inflammation through upregulation of IL-10 and downregulation of TNF-α. To test this hypothesis, 8 week old, female C57BL/6J mice were fed with HFD and exercised (swimming 1 h/day for 5 days/week for 8 weeks). The four treatment groups: normal diet (ND), HFD, HFD + exercise (HFD + Ex) and ND + Ex were analyzed for mean body weight, blood glucose level, TNF-α, IL-10, cardiac fibrosis by Masson Trichrome, and cardiac dysfunction by echocardiography. Mean body weights were increased in HFD but comparatively less in HFD + Ex. The level of TNF-α was elevated and IL-10 was downregulated in HFD but ameliorated in HFD + Ex. Cardiac fibrosis increased in HFD and was attenuated by exercise in the HFD + Ex group. The percentage ejection fraction and fractional shortening were decreased in HFD but comparatively increased in HFD + Ex. There was no difference between ND and ND + Ex for the above parameters except an increase in IL-10 level following exercise. Based on these results, we conclude that exercise mitigates HFD- induced cardiomyopathy by decreasing obesity, inducing IL-10, and reducing TNF-α in mice.
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