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维生素 C 通过减少氧化应激,诱导 TM4 支持细胞中 HSP 的表达,从而减轻热损伤。

Vitamin C mitigates heat damage by reducing oxidative stress, inducing HSP expression in TM4 Sertoli cells.

机构信息

Department of Veterinary Pathology, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.

出版信息

Mol Reprod Dev. 2019 Jun;86(6):673-685. doi: 10.1002/mrd.23146. Epub 2019 Apr 15.

DOI:10.1002/mrd.23146
PMID:30989754
Abstract

Heat stress is a major stressor that can lead to male reproductive dysfunction. Sertoli cells play a crucial role in spermatogenesis by providing germ cells with structural and nutritional support, and contributing to blood-testis barrier formation. Vitamin C (Vc) is an antioxidant capable of neutralizing reactive oxygen species and preventing lipid peroxidation widely used because it is inexpensive and highly accessible. In the present study, we investigated the protective effect of Vc on TM4 cells following heat stress. Pretreatment with Vc could effectively inhibit apoptosis (p < 0.01), lipid peroxidation, and lactate dehydrogenase (LDH) activity. However, a significant increase in the malondialdehyde (MDA) level and LDH activity (p < 0.01) was observed in TM4 cells without Vc-pretreatment, in conjunction with vacuole degeneration and karyopyknosis. In addition, both the messenger RNA and protein levels of CryAB, Hsp27, Hsp70, and Hsp110 substantially increased in the 3 and 12 hr recovery groups (p < 0.01). Vc also prevented microtubule aggregation following heat stress. These results suggest that pretreatment with Vc-protected TM4 cells against heat stress by reducing the level of oxidative stress and inducing heat shock protein expression.

摘要

热应激是导致男性生殖功能障碍的主要应激源。支持细胞通过为生殖细胞提供结构和营养支持,并有助于血睾屏障的形成,在精子发生中起着至关重要的作用。维生素 C(Vc)是一种抗氧化剂,能够中和活性氧并广泛用于防止脂质过氧化,因为它价格低廉且易于获得。在本研究中,我们研究了 Vc 对热应激后 TM4 细胞的保护作用。Vc 预处理可有效抑制细胞凋亡(p<0.01)、脂质过氧化和乳酸脱氢酶(LDH)活性。然而,在没有 Vc 预处理的情况下,TM4 细胞的丙二醛(MDA)水平和 LDH 活性显著升高(p<0.01),同时还观察到空泡变性和核固缩。此外,在 3 和 12 小时恢复组中,CryAB、Hsp27、Hsp70 和 Hsp110 的信使 RNA 和蛋白水平均显著增加(p<0.01)。Vc 还可以防止热应激后微管聚集。这些结果表明,Vc 预处理通过降低氧化应激水平和诱导热休克蛋白表达来保护 TM4 细胞免受热应激。

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