Calorie restriction protects against apoptosis, mitochondrial oxidative stress and increased calcium signaling through inhibition of TRPV1 channel in the hippocampus and dorsal root ganglion of rats

Calorie restriction protects against apoptosis, mitochondrial oxidative stress and increased calcium signaling through inhibition of TRPV1 channel in the hippocampus and dorsal root ganglion of rats
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DOI:
10.1007/s11011-018-0289-0
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发表时间:
2018-10-01
影响因子:
3.6
通讯作者:
Cig, Bilal
Cig, Bilal
中科院分区:
医学3区
文献类型:
--
作者:
Gultekin, Fatih;Naziroglu, Mustafa;Cig, Bilal

文献摘要

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TRPV1通道在神经元中被辣椒素、氧化应激、酸性pH和热因素激活,而这些因素被卡路里限制(CR)的抗氧化作用减弱。因此,我们研究了CR和食物频率(FF)的抗氧化作用可能通过抑制海马(HIPPON)和背根神经节神经元(DRGN)线粒体氧化应激来调节TRPV1活性和细胞凋亡的假设。我们研究了FF和CR通过抑制TRPV1对大鼠神经元损伤和凋亡的作用。我们将大鼠分为对照组、FF组和FF + CR组。对照组和FF组分别补充一定量的自由采食,持续20周。FF + CR组饲喂与对照组相同的食物量,但同期热量减少20%。主要结果发现,FF处理后,hipon和DRGN中的TRPV1电流、细胞内Ca2+水平、凋亡、活性氧、线粒体去极化、PARP-1表达、caspase 3和9活性和表达值升高,而FF + CR处理后,这些影响减弱。FF + DR处理显著降低了相同样品的脂质过氧化水平,但显著降低了HIPPO和DRGN的细胞活力,提高了HIPPO、DRGN、血浆、肝脏和肾脏的维生素E浓度、谷胱甘肽过氧化物酶、维生素A和β -胡萝卜素的含量。综上所述,CR通过TRPV1降低了ff诱导的hipon和DRGN中氧化应激、细胞凋亡和Ca2+进入的增加。我们的发现可能与CR治疗后肥胖的病因和治疗有关。
The TRPV1 channel is activated in neurons by capsaicin, oxidative stress, acidic pH and heat factors, and these factors are attenuated by the antioxidant role of calorie restriction (CR). Hence, we investigated the hypothesis that the antioxidant roles of CR and food frequency (FF) may modulate TRPV1 activity and apoptosis through inhibition of mitochondrial oxidative stress in hippocampal (HIPPON) and dorsal root ganglion neurons (DRGN). We investigated the contribution of FF and CR to neuronal injury and apoptosis through inhibition of TRPV1 in rats. We assigned rats to control, FF and FF + CR groups. A fixed amount of food ad libitum was supplemented to the control and FF groups for 20 weeks, respectively. FF + CR group were fed the same amount of food as the control group but with 20% less calories during the same period. In major results, TRPV1 currents, intracellular Ca2+ levels, apoptosis, reactive oxygen species, mitochondrial depolarization, PARP-1 expression, caspase 3 and 9 activity and expression values were found to be increased in the HIPPON and DRGN following FF treatment, and these effects were decreased following FF + CR treatment. The FF-induced decrease in cell viability of HIPPO and DRGN, and vitamin E concentration of brain, glutathione peroxidase, vitamin A, and beta-carotene values of the HIPPO, DRGN, plasma, liver and kidney were increased by FF + DR treatment, although lipid peroxidation levels in the same samples were decreased. In conclusion, CR reduces FF-induced increase of oxidative stress, apoptosis and Ca2+ entry through TRPV1 in the HIPPON and DRGN. Our findings may be relevant to the etiology and treatment of obesity following CR treatment.