Study of Plasma Corticosterone Upon Chronic Stress Induction and Its Effect on Follicular Development in Rattus norvegicus

Nitin Kalsi Rajashekara, Bindu Jayashankaraswamy, Raghu Nataraj


Background: Sex hormones controlling the ovarian function are centrally controlled by the hypothalamus, and the downstream control are carried through the pituitary secretion via the hypothalamus-pituitary-gonadal (HPG) axis. In rodents, corticosterone under stress conditions is known to disrupt the hormones of HPG axis at multiple stages and exhibits pathological impact on ovaries. The current study aimed to investigate the role of chronic stress effect on the regulation of corticosterone and its counter effectiveness in dysregulating testosterone, estradiol levels, along with the interference in ovarian follicular development and polycystic ovary syndrome (PCOS) induction in Rattus norvegicus.

Methods: The study identified the rat models into three groups, i.e., control, stress and stress with ketoconazole treated. The high dosage of ketoconazole exhibits the corticosterone suppression effect. Control animals were left undisturbed and maintained under standard conditions. Stress group animals were exposed to different stress induction parameters such as restraining, dark shift, forced swimming, acute heat, and social isolation. Another stress group of animals were treated with 50 mg/kg body weight of ketoconazole prior to the stress exposure which was conducted for 30 days. At the end of stress observations, animals were euthanized, ovaries collected, stored in neutral buffer formalin for further histopathology studies and the plasma was collected and stored under -20 C for further hormonal investigations.

Results: The study demonstrates a significant increase in number of days per estrous cycle among the stress group animals by vaginal cytology analysis. Histopathology study of ovaries revealed healthy follicular development in control group of animals and cystic follicular growth among the stress group animals. Animals treated with 50 mg/kg body weight ketoconazole exhibited improper follicular growth. All the study observations were correlated with the hormonal estimations across the animal groups against Rotterdam criteria and the results inferred.

Conclusions: Our observation is that damaged impaired folliculogenesis which has led to ovarian failure may be imputed to change in hormonal secretion pattern.

J Endocrinol Metab. 2023;13(3):114-120


Stress; Ketoconazole; Corticosterone; Testosterone; Estradiol; Polycystic ovary syndrome

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