Abstract
Objective The present study is aimed at investigating the anti-inflammatory, antioxidative, and antiapoptotic effects of methane on lipopolysaccharide- (LPS-) induced acute orchitis and its potential mechanisms. Methods Adult male rats were intraperitoneally (i.p.) injected with methane-rich saline (MS, 20 mL/kg) following LPS (5 mg/kg, i.p.). The survival rate was assessed every 12 h until 72 h after LPS induction, and surviving rats were sacrificed for further detection. The wet/dry (W/D) ratio was determined, and testicular damage was histologically assessed. Inflammatory cytokines in the testes and serum, including interleukin-1β (IL-1β), IL-6, IL-10, and tumor necrosis factor-α (TNF-α), were measured using ELISA and RT-qPCR. Oxidative stress was evaluated by the level of superoxide dismutase (SOD) and malondialdehyde (MDA). Testicular apoptosis was detected via TUNEL staining. The expression of prokineticin 2 (PK2)/prokineticin receptor 1 (PKR1) was also analyzed using RT-qPCR, western blotting, and immunohistochemistry. Results It was found that methane significantly prolonged rat survival, decreased the W/D ratio, alleviated LPS-induced histological changes, and reduced apoptotic cells in the testes. Additionally, methane suppressed and promoted the production of pro- and anti-inflammatory cytokines, respectively. Furthermore, methane significantly increased SOD levels, decreased MDA levels, and decreased testicular expression of PK2 and PKR1. Therefore, methane exerts therapeutic effects on acute orchitis and might be a new and convenient strategy for the treatment of inflammation-related testicular diseases.
Highlights
It has been reported that infertility, including male infertility, affects ~16% of couples worldwide and is relatively prevalent in clinic [1]
It has been proved that the pathogenesis of orchitis mainly includes inflammatory cytokine imbalance, oxidative stress, apoptosis, and prokineticin 2 (PK2)/prokineticin receptor 1 (PKR1) pathway
Increasing evidences indicate that the imbalance among these pro- and anti-inflammatory molecules, such as interleukin-1β (IL1β), IL-6, tumor necrosis factor-α (TNF-α), and IL-10, in testicular cells can result in orchitis [3, 4]
Summary
It has been reported that infertility, including male infertility, affects ~16% of couples worldwide and is relatively prevalent in clinic [1]. Recent researches have demonstrated that infection and inflammation of the testes are one of the major contributors to male infertility, accounting for ~15% of cases of male infertility [2]. It has been proved that the pathogenesis of orchitis mainly includes inflammatory cytokine imbalance, oxidative stress, apoptosis, and prokineticin 2 (PK2)/prokineticin receptor 1 (PKR1) pathway. Increasing evidences indicate that the imbalance among these pro- and anti-inflammatory molecules, such as interleukin-1β (IL1β), IL-6, tumor necrosis factor-α (TNF-α), and IL-10, in testicular cells can result in orchitis [3, 4]. Oxidative stress and reactive oxygen species (ROS), which are majorly sourced from macrophages [5], may be the major contributory
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