Simple Summary
In sheep farming, ovarian inflammation caused by bacterial infections often leads to infertility and economic losses. Bacterial toxins damage the ovarian cells that support egg development, but whether selenium, a trace mineral with recognized anti-inflammatory properties, can protect these cells remains unclear. In this study, we exposed sheep ovarian cells to bacterial toxin to induce inflammation and then treated them with selenium. Using high-resolution microscopy and functional assays, we found that the toxin severely damaged the mitochondria—the energy-producing compartments of the cells—causing them to shrink and fragment. Selenium treatment restored these structures to a healthy state. This structural repair, in turn, reduced inflammation and cell death, alleviated oxidative stress, and improved the production of reproductive hormones by the cells. Our findings provide direct evidence that selenium protects sheep ovarian cells by preserving their internal structures, suggesting that selenium supplementation could serve as a practical nutritional strategy for safeguarding sheep fertility against inflammation-related disorders.
Abstract
Lipopolysaccharide (LPS) impairs the function of ovine follicular granulosa cells (GCs), representing a primary cause of follicular atresia. Selenium (Se), an essential trace element, possesses anti-inflammatory and cytoprotective properties; however, its effects on GC ultrastructure remain largely unknown. In this study, primary ovine GCs were exposed to LPS (10 µg/mL) and treated with sodium selenite (25 nM). Transmission electron microscopy (TEM), JC-1 staining, enzyme-linked immunosorbent assay (ELISA), reactive oxygen species (ROS) detection, flow cytometry, and quantitative real-time PCR (qRT-PCR) were employed to evaluate cellular ultrastructure, mitochondrial membrane potential (ΔΨm), and downstream physiological processes. LPS induced severe mitochondrial pyknosis, cristae loss, and reduced ΔΨm, accompanied by inflammation, oxidative stress, apoptosis, and impaired steroidogenesis. Se intervention markedly ameliorated these ultrastructural injuries, preserving mitochondrial morphology and ΔΨm. Functionally, Se suppressed the release of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β); enhanced the activities of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) while attenuating ROS accumulation; inhibited apoptosis by upregulating BCL-2 and downregulating BAX and CASPASE-3; and restored E2 and P4 secretion via upregulation of STAR and NR5A1. This study provides direct morphological evidence that Se protects ovine GCs from LPS-induced damage by repairing mitochondrial ultrastructure. This structural restoration is central to its integrated anti-inflammatory, antioxidant, anti-apoptotic, and steroidogenic effects. These in vitro findings suggest that Se may serve as a promising nutritional strategy for mitigating inflammation-driven follicular atresia, pending further in vivo validation.
Keywords:
ovine; GCs; selenium; mitochondrial ultrastructure; inflammation; oxidative stress; apoptosis; steroidogenesis