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首页> 外文期刊>Journal of cellular physiology. >SIRT3 mitigates intervertebral disc degeneration by delaying oxidative stress-induced senescence of nucleus pulposus cells
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SIRT3 mitigates intervertebral disc degeneration by delaying oxidative stress-induced senescence of nucleus pulposus cells

机译：SIRT3减轻椎间盘变性通过延迟衰老氧化应激髓核细胞的

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摘要

Senescence of nucleus pulposus (NP) cells (NPC) is a major cause of intervertebral disc degeneration (IVDD), so delay NPC senescence may be beneficial for mitigating IVDD. We studied the effect and mechanism of silent information regulator 2 homolog 3 (SIRT3) on NPC senescence in vivo and in vitro. First, we observed SIRT3 expression in normal and degenerated NPC with immunohistochemical and im-munofluorescence staining. Second, using SIRT3 lentivirus transfection, reactive oxygen species probe, senescence-associated (3-galactosidase staining, polymerase chain reaction, and western blot to observe the oxidative stress, senescence, and degeneration degree among groups. Subsequently, pretreatment with adenosine monophosphate-activated protein kinase (AMPK) agonists and inhibitors, observing oxidative stress, senescence, and degeneration degree among groups. Finally, the IVDD model was constructed and divided into Ctrl, Vehicle, LV-shSIRT3, and LV-SIRT3 groups. X-ray and magnetic resonance imaging scans were performed on rat's tails after 1 week; hematoxylin and eosin and safranin-O staining were used to evaluate the degree of IVDD; immunofluorescence staining was used to observe SIRT3 expression; immunohistochemical staining was used to observe oxidative stress, senescence, and degeneration degree of NP. We found that SIRT3 expression is reduced in degenerated NP tissues but increased in H2O2-induced NPC. Moreover, SIRT3 upregulation decreased oxidative stress, delayed senescence, and degeneration of NPC. In addition, activation of the AMPK/PGC-la pathway can partially mitigate the NPC oxidative stress, senescence, and degeneration caused by SIRT3 knockdown. The study in vivo revealed that local SIRT3 overexpression can significantly reduce oxidative stress and ECM degradation of NPC, delay NPC senescence, thereby mitigating IVDD. In summary, SIRT3 mediated by the AMPK/PGC-la pathway mitigates IVDD by delaying oxidative stress-induced NPC senescence.
机译：衰老的髓核细胞(NPC) (NP)椎间盘退化的主要原因(类),所以延迟人大衰老可能是有益的为减轻类。无声的信息监管机制2同族体3 (SIRT3)在体内和人大衰老体外。正常的和退化人大免疫组织化学和im-munofluorescence染色。转染,活性氧探针,senescence-associated (3-galactosidase染色,聚合酶链反应和免疫印迹观察氧化应激、衰老和变性程度组间。与腺苷预处理monophosphate-activated蛋白激酶(AMPK)受体激动剂和抑制剂,观察氧化压力、衰老和退化程度中组。车辆,分为Ctrl LV-shSIRT3,LV-SIRT3组。成像扫描进行老鼠的尾巴1周;染色是用来评估的程度类;观察SIRT3表达式;染色是用来观察氧化应激,衰老和退化程度的NP。发现,SIRT3表达减少但增加组织退化NPH2O2-induced人大。减少氧化应激,推迟衰老,和人大变性。AMPK / PGC-la途径可以部分缓解全国人大氧化应激、衰老和变性所致,SIRT3击倒。体内透露,当地SIRT3超表达可以显著降低氧化应激和ECM吗人大退化,从而延迟人大衰老,减轻类。AMPK / PGC-la途径减轻类延缓氧化应激人大衰老。

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