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The ameliorate effect of 18-beta glycyrrhetinic acid against cadmium-induced reproductive damage
Osman Çiftçi1, Münevver Nazlıcan Kaplan2, Özlem Özmen3
1Faculty of Medicine, Department of Medical Pharmacology, Pamukkale University, 20190, Denizli, Turkey. ociftci@pau.edu.tr.
Abstract:
This study aimed to investigate whether 18β-glycyrrhetinic acid (GA) could protect against cadmium-induced testicular damage in male rats. Twenty-four adult male Sprague Dawley rats were randomly divided into four groups (n = 6): Control, Cadmium (CAD), GA, and Cadmium + GA. Cadmium and GA were administered at doses of 1 mg/kg and 100 mg/kg, respectively, for 50 days. At the end of the experimental period, testicular and epididymal tissues were collected for biochemical, molecular, histopathological, and immunohistochemical analyses. Biochemical evaluations included oxidative stress parameters (TAS, TOS) and inflammatory cytokines (TNF-α, IL-6). Apoptotic gene expression (Bcl-2, Bax, Caspase-3) was assessed by RT-PCR. Histopathological and immunohistochemical analyses were performed to evaluate Bcl-2, Bax, iNOS, and NF-κB expression. Cadmium exposure significantly increased oxidative stress and inflammatory cytokine levels and induced marked histological damage, including Leydig cell necrosis and severe tubular degeneration. Immunohistochemical analysis revealed increased Bax, iNOS, and NF-κB expression in testicular and epididymal tissues. Cadmium also upregulated Bax and Caspase-3 while downregulating Bcl-2 gene expression. Conversely, GA treatment significantly attenuated cadmium-induced oxidative stress, inflammation, apoptosis, and histological damage. These findings suggest that GA exerts protective effects against cadmium-induced testicular toxicity and may represent a promising therapeutic agent for preventing cadmium-related male infertility.
Insights
18β-glycyrrhetinic acid (GA) protects male rats from cadmium-induced testicular damage. GA treatment reduced oxidative stress, inflammation, and apoptosis, suggesting its potential for preventing male infertility.
Area of Science:
- Reproductive Toxicology
- Pharmacology
- Biochemistry
Background:
- Cadmium (CAD) exposure is a known cause of male reproductive toxicity.
- Oxidative stress, inflammation, and apoptosis are key mechanisms in cadmium-induced testicular damage.
- 18β-glycyrrhetinic acid (GA) is a natural compound with potential therapeutic properties.
Purpose of the Study:
- To investigate the protective effects of GA against cadmium-induced testicular damage in male rats.
- To elucidate the underlying mechanisms of GA's protective action.
Main Methods:
- Male Sprague Dawley rats were exposed to cadmium (1 mg/kg) with or without GA (100 mg/kg) for 50 days.
- Evaluations included biochemical assays (oxidative stress, cytokines), gene expression analysis (apoptosis markers), and histopathological/immunohistochemical assessments.
Main Results:
- Cadmium exposure significantly increased oxidative stress, inflammation (TNF-α, IL-6), and apoptosis (Bax, Caspase-3 upregulation; Bcl-2 downregulation).
- Histopathology revealed Leydig cell necrosis and tubular degeneration in cadmium-exposed rats.
- GA treatment significantly reversed these cadmium-induced changes, reducing oxidative stress, inflammation, apoptosis, and histological damage.
Conclusions:
- GA demonstrates significant protective effects against cadmium-induced testicular toxicity in male rats.
- GA attenuates cadmium's adverse effects by mitigating oxidative stress, inflammation, and apoptosis.
- GA may serve as a promising therapeutic agent for cadmium-related male infertility.