Background: Follicle development takes place under the control of hormonal and environmental stimuli. It suggested that to improve in vitro fertilisation outcomes in poor responders increasing gonadotropin doses be used. Excessive gonadotropin leads to atresia and impairs follicular development, but the molecular mechanisms of follicular atresia remain largely unknown. Recently, it was suggested that autophagy may be an alternative mechanism involved in follicle depletion. Aims: In this study, we aimed to clarify the role of autophagic markers such as light chain (LC) 3B and voltage dependent anion channel 2 (VDAC2) in follicular atresia using the high dose gonadotropin stimulation. Settings and Design: The female 24 BALB/c mice were employed in the present study under the Committee for the Purpose of Control and Supervision of Experiments on Animals guidelines with ethical clearance from the institutional ethical committee. These mice were categorised into four groups, with six rats in each as control and test animals. Materials and Methods: Group 1 (control): no action will be taken. Group 2 (sham): only saline will be applied. Group 3: low-dose gonadotropin Pregnant mare's serum gonadotropin (PMSG) + human chorionic gonadotropin (HCG) will be applied. Group 4: high-dose gonadotropin + HCG will be applied. The animals were sacrificed 48 h after the last injection. For all group samples, both protein and mRNAs of the LC3B and VDAC2 were examined by immunohistochemical and reverse transcription-polymerase chain reaction techniques. Statistical Analysis Used: All variables were analysed using GraphPad Prism 8. Kruskal–Wallis t-test and Mann–Whitney U test were used to compare immunohistochemical results; in addition to this, parametric one-way ANOVA test and Shapiro–Wilk test were applied for quantitative polymerase chain reaction statistics. Results: An increased number of atretic follicles were observed in the high-dose gonadotropin + HCG group. LC3B immunoreactivity of the atretic secondary follicles in the high-dose group is higher than in other groups. The expression of VDAC2 protein in the secondary and Graafian follicles and also VDAC2 mRNA in the ovary were more highly expressed in the control and sham groups. The decrease in VDAC2 mRNA level and immunohistochemical expression was remarkable in the low-dose and high-dose follicle-stimulating hormone groups compared to the control and sham groups. Conclusion: In this study, the increased LC3B and decreased VDAC2 expression, which are autophagy markers, were observed in both the gonadotropins groups, so we suggested that high doses of gonadotropins may cause ovarian atresia.

Aim: Duchenne Muscular Dystrophy (DMD) results in a deficiency of dystrophin expression in patient muscle fibers, leading to progressive muscle degeneration. Treatment of DMD has undertaken current transformation with the advancement of novel gene therapy and molecular biology techniques, which are secure, well-tolerated, and effective therapeutic approaches. Introduction: DMD gene therapies have mainly focused on young DMD patients as in vivo animal model trials have been performed in 0–1-month DMD mice. However, it has not yet been answered how micro-dystrophin encoding lentiviral treatment affects Dystrophin expression and DMD symptoms in 10-month mdx mice. Methods: We planned to integrate the micro-Dystrophin gene sequence into the muscle cells by viral transfer, using micro-Dystrophin-encoding lentivirus to reduce the dystrophic pathology in late-stage dmd mice. The histopathological and physiological-functional regeneration activities of the lentiviral-micro-Dystrophin gene therapy methods were compared, along with changes in temporal Dystrophin expression and their functionality, toxicity, and gene expression level. method: We planned to integrate the micro-Dystrophin gene sequence into the muscle cells by viral transfer, using micro-Dystrophin-encoding lentivirus to reduce the dystrophic pathology in late-stage dmd mice. The histopathological and physiological-functional regeneration activities of the lentiviral-micro-Dystrophin gene therapy methods were compared, along with changes in temporal Dystrophin expression and their functionality, toxicity, and gene expression level. Results: Here, we showed that the micro-dystrophin transgene transfers intramuscularly and intraperitoneally in late-stage dmd-mdx-4cv mice restored dystrophin expression in the skeletal and cardiac muscle (p <0.001). Furthermore, motor performance analysis, including hanging and tracking tests, improved statistically significantly after the treatment (p <0.05). Conclusion: Consequently, this study suggests that patients in the late stages of muscular dystrophy can benefit from lentiviral micro-dystrophin gene therapies to present an improvement in dystrophic muscle pathology. conclusion: Consequently, this study suggests that patients in the late stages of muscular dystrophy can benefit from the lentiviral micro-dystrophin gene therapies to present an improvement in dystrophic muscle pathology.