HO-1 reduces heat stress-induced apoptosis in bovine granulosa cells by suppressing oxidative stress

Abstract

Heat stress negatively affects reproduction in cattle by disrupting the normal function of ovarian granulosa cells (GCs), ultimately leading to oxidative damage and cell death via apoptosis. Heme oxygenase-1(HO-1) is a member of the heat shock protein family, which are associated with cellular antioxidant defenses and anti-apoptotic functions. Recent studies demonstrated that HO-1 is upregulated in heat-stressed cells. In the present study, we investigated the expression of HO-1 in bovine GCs transiently exposed to heat stress and characterized the expression and activity of key oxidative stress enzymes and molecules. We show that heat stress induced oxidative stress and apoptosis, and enhanced Nrf2 and HO-1 expression in primary GC cultures. Knocking down HO-1 expression using siRNA exacerbated both oxidative stress and apoptosis, whereas pre-treating GCs with hemin, which induces HO-1 expression, partially prevented these effects. These findings demonstrate that HO-1 attenuates heat stress-induced apoptosis in bovine GCs by decreasing production of reactive oxygen species and activating the antioxidant response.

Pterostilbene Alleviates Aβ1‐42‐Induced Cognitive Dysfunction via Inhibition of Oxidative Stress by Activating Nrf2 Signaling Pathway

“…[ 10,11 ] Studies showed that HO‐1 was able to resist oxidative stress. [ 44 ] Activation of HO‐1 could reduce Aβ 1‐42 toxicity. [ 45,46 ] SOD catalyzes the disproportionation of superoxide anion radicals to form oxygen and hydrogen peroxide, thereby maintaining redox balance.…”

The Role of Oxidative Stress and Natural Antioxidants in Ovarian Aging

“…The effector, caspase-3, executes the final steps of apoptosis and cleaves various structural and regulatory proteins in female germ cells ( Xiong et al, 2014 ). Li et al demonstrated that oxidative stress induced bovine GC apoptosis by increasing the expression of cleaved caspase-3 and the Bax/Bcl-2 ratio as well as decreasing the expression of antioxidant enzymes (SOD2, glutathione peroxidase (GSH-Px)) ( Wang Y et al, 2019 ). In addition, excessive ROS in oocytes and GCs can induce the release of TNFα ( Kong et al, 2018 ; Miao et al, 2018 ).…”

PERK-Mediated eIF2α Phosphorylation Contributes to The Protection of Dopaminergic Neurons from Chronic Heat Stress in Drosophila

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