Abstract
The cross-talk between oocyte and somatic cells plays a crucial role in the regulation of follicular development and oocyte maturation. As a result, granulosa cell apoptosis causes follicular atresia. In this study, sheep granulosa cells were cultured under thermal stress to induce apoptosis, and melatonin (MT) was examined to evaluate its potential effects on heat-induced granulosa cell injury. The results demonstrated that the Colony Forming Efficiency (CFE) of granulosa cells was significantly decreased (heat 19.70% ± 1.29% vs. control 26.96% ± 1.81%, p < 0.05) and the apoptosis rate was significantly increased (heat 56.16% ± 13.95%vs. control 22.80% ± 12.16%, p < 0.05) in granulosa cells with thermal stress compared with the control group. Melatonin (10−7 M) remarkably reduced the negative effects caused by thermal stress in the granulosa cells. This reduction was indicated by the improved CFE and decreased apoptotic rate of these cells. The beneficial effects of melatonin on thermal stressed granulosa cells were not inhibited by its membrane receptor antagonist luzindole. A mechanistic exploration indicated that melatonin (10−7 M) down-regulated p53 and up-regulated Bcl-2 and LHR gene expression of granulosa cells under thermal stress. This study provides evidence for the molecular mechanisms of the protective effects of melatonin on granulosa cells during thermal stress.
Highlights
Thermal stress disrupts spermatogenesis, follicle development, oocyte maturation, early embryonic development, fetal and placental growth and lactation
Following melatonin (10−7 M) treatment, the Colony Forming Efficiency (CFE) of both the thermal stressed and control groups were significantly increased compared with their melatonin-free counterparts (p < 0.05)
The percentage of apoptotic cells in the thermal stressed group with 10−7 M melatonin was significantly lower than the group without melatonin, and it was not significantly different (p > 0.05) from the control group
Summary
Thermal stress disrupts spermatogenesis, follicle development, oocyte maturation, early embryonic development, fetal and placental growth and lactation. It has negative impacts on human health and causes serious problems in the livestock industry [1]. ROS formation and elimination is a dynamic balance Thermal stress disturbs this balance and promotes ROS production in cells, which, in turn, causes cellular oxidative stress [2]. These effects include DNA, protein and lipid damage, which leads to cell apoptosis or necrosis [3,4].
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