Kisspeptin is a neuropeptide encoded by the kisspeptin gene (Kiss1) and located in different brain regions, primarily in the hypothalamus. Kisspeptin and its receptor G-protein-coupled receptor-54 (GPR54), are also found in behavioural brain regions such as the hippocampus and cortex. Kisspeptin, a very powerful neuropeptide that stimulates the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary, does this by increasing gonadotropin-releasing hormone (GnRH) levels. In recent studies, it has been noted that kisspeptin is effective on reproductive functions. Globally 8 to 12% of couples have infertility problems, and the majority are residents of developing countries. Approximately 70% of infertility cases are caused by fertility problems in women. The frequency of infertility in women continues to increase every year and the underlying factors require further research. Bearing this problem in mind, this review examines the possible role of kisspeptin in female infertility. In doing so, it aims to find out how future application of kisspeptin may potentially unravel the neural reproductive disorder.

In our study, the potential protective effects of boric acid (BA) against ovarian damage induced by 3-nitropropionic acid (3-NPA) were investigated. In an experiment conducted on female Wistar rats, the animals were divided into groups receiving control, 3-NPA, 3-NPA + BA, and BA only. 3-NPA triggers oxidative stress in the body by inducing excessive production of reactive oxygen species (ROS), leading to cellular damage and apoptosis. Experimental results showed that oxidative stress markers (MDA, GSH, and GSH-Px) increased in the group treated with 3-NPA, along with elevated inflammatory and apoptotic indicators (TNF-α, IL-6, NF-κB, caspase 3, and 9). Moreover, significant histopathological findings such as degeneration, necrosis, and oocyte loss in follicles were observed. Boric acid application significantly reduced these adverse effects, enhancing antioxidant defense and providing protective effects on ovarian tissue. In conclusion, it was observed that BA’s antioxidant and anti-apoptotic properties exhibited protective potential against 3-NPA-related ovarian damage, with a positive impact on reproductive health. The study suggests that BA might be used as a supportive agent in diseases of the female reproductive system.

The stimulation of the TRPV1 channel through capsaicin (CAP) and oxidative stress induces increases of 3‐Nitropropionic acid (3NPA)‐induced brain and hippocampus injury, whereas its inhibition by antioxidant silymarin (SIL) and capsazepine (CPZ) may suppress the increases in the brain and hippocampus injury. The antioxidant and antiapoptotic actions of SIL were investigated in the HT‐22 mouse hippocampal cells and the brain of mice by diminishing the TRPV1 signaling pathways. A total of 32 mice were equally divided into four groups: control, SIL (100 mg/kg/day), 3NPA (12.5 mg/kg and single dose), and 3NPA + SIL. Mouse hippocampal HT‐22 cells were also divided into four groups: control, SIL (10 µM for 24 h), 3NPA (1 mM for 24 h), and 3NPA + SIL. The 3NPA‐induced increases of apoptotic (caspases‐3, ‐8, and ‐9) and oxidant (mitochondrial reactive oxygen species (mROS), mitochondrial membrane dysfunction, and lipid peroxidation) markers were decreased through upregulation of glutathione, glutathione peroxidase, retinol, alpha‐tocopherol, and beta‐carotene in the brain of mice by the SIL and CPZ treatments. In the HT‐22 cells, the 3NPA‐induced increases of Ca ²⁺ , mROS, TRPV1 current densities, and death cell percentage were decreased in 3NPA + SIL and 3NPA + CPZ groups by the SIL and CPZ treatments, although the decreases of HT‐22 viability were increased by the treatments. These findings suggest that silymarin‐associated inhibition of TRPV1 signaling is consistent with a neuroprotective role against 3NPA‐induced neurotoxicity, though TRPV1‐independent mechanisms cannot be excluded.

This study aimed to investigate the effects of active anionic oxygen (AAO) on oxidative stress, inflammation, and steroidogenesis in sepsis-induced testicular injury in rats. Thirty male Wistar Albino rats were randomly assigned to four groups: Control, Sepsis (lipopolysaccharide, LPS), AAO, and Sepsis+AAO. Testicular tissues were analyzed for oxidative stress markers (reduced glutathione [GSH], malondialdehyde [MDA], superoxide dismutase [SOD], and catalase [CAT]), inflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-α], transforming growth factor-beta 1 [TGF-β1], and interleukin-1 beta [IL-1β]), and steroidogenic markers (3β-hydroxysteroid dehydrogenase [3β-HSD], 17β-hydroxysteroid dehydrogenase [17β-HSD], and steroidogenic acute regulatory protein [StAR]). Sepsis significantly decreased GSH (p < .0001), SOD (p < .01), and CAT (p < .0001) levels, while increasing MDA (p < .0001) levels compared with the control group. In addition, IL-6 (p < .0001), TNF-α (p < .001), TGF-β1 (p < .05), and IL-1β (p < .0001) levels were significantly elevated, whereas the expression of 3β-HSD (p < .01), 17β-HSD (p < .05), and StAR (p < .01) was significantly reduced. Compared with the sepsis group, AAO treatment significantly improved antioxidant status (all p < .05), suppressed inflammatory cytokine levels (all p < .01), and enhanced steroidogenic marker expression (all p < .05). These findings demonstrate that AAO exerts potent antioxidant and anti-inflammatory effects, attenuates sepsis-induced testicular injury, and preserves steroidogenesis, suggesting its potential as a protective agent for sepsis-associated testicular dysfunction.

Background: Sepsis is a life-threatening systemic condition characterized by organ dysfunction resulting from a dysregulated host response to infection. This study aimed to investigate the protective role of juglone (5-hydroxy-1,4-naphthoquinone), a naturally occurring compound, on lung tissue in a cecal ligation and puncture (CLP)-induced sepsis model. Methods: Male Wistar-albino rats were used to establish the model, and juglone was administered intraperitoneally at doses of 1, 2, and 3 mg/kg. Lung and serum samples were collected for biochemical, molecular, and histological analyses through ELISA, RT-PCR, Western blot, and histopathological examinations. Results: In the sepsis group, the levels of proinflammatory cytokines (IL-1β, IL-6, IL-18) and pyroptosis-related markers (NLRP3, caspase-1, GSDMD) were significantly elevated, while juglone pretreatment markedly reduced these parameters in a dose-dependent manner. Moreover, juglone upregulated the Nrf2/HO-1 antioxidant pathway while downregulating Keap1 expression. RT-PCR analysis revealed that juglone suppressed the expression of pro-apoptotic genes (caspase-3, caspase-9, Bax) and enhanced anti-apoptotic Bcl-2 expression. Histopathological evaluation demonstrated that juglone alleviated inflammatory cell infiltration, septal thickening, and hemorrhage in lung tissue. Conclusions: These findings suggest that juglone is associated with protection against sepsis-induced lung injury and with changes in oxidative stress, inflammation, apoptosis, and pyroptosis pathways. Therefore, juglone may have protective potential against sepsis-induced pulmonary damage.

Nicotine exposure can disrupt redox homeostasis and damage the male reproductive system. This study evaluated short-term nicotine-associated systemic and testicular changes and examined whether concurrent silymarin treatment attenuated these alterations. Twenty-eight adult male Swiss albino mice were randomized to control, nicotine, silymarin, and nicotine plus silymarin groups (n = 7 each). Nicotine (1.5 mg/kg/day) and silymarin (100 mg/kg/day) were administered intraperitoneally for seven days. Whole-blood glutathione, plasma malondialdehyde, superoxide dismutase, nitric oxide, paraoxonase-1, total sialic acid, lipid profile, caspase-3, and nuclear factor kappa B, testicular redox markers, and testicular histomorphology were assessed. Nicotine was associated with lower blood glutathione and plasma superoxide dismutase and paraoxonase-1 activities, higher plasma malondialdehyde, nitric oxide, total sialic acid, caspase-3, and nuclear factor kappa B values, and an unfavorable testicular redox profile (all p < 0.001). Degenerative changes were also observed in seminiferous tubules and Leydig cells. Concurrent silymarin treatment attenuated most biochemical alterations and was associated with less severe histological injury, although several markers did not fully return to control values. These findings support a partial protective association under the conditions tested; reproductive function was not directly assessed.