Abstract
Objective: To study the effect of Yu Linzhu on ovarian function and mitochondria in natural aging mice.Methods: Female BALB/c mice were selected as normal group at 7–8 weeks and natural aging group at 9 months. The natural aging group was divided into Yu Linzhu intervention group and non-intervention group by intragastric administration once a day for 6 weeks. The morphology and blood flow of ovary were observed by ultrasound. Ovarian morphology and follicle were observed by HE staining. Hormone levels were analyzed by ELISA. Serum oxidative stress were detected by radioimmunoassay. The distribution of mitochondria in oocytes was observed by fluorescence staining. The ultrastructure of oocytes and the morphology of mitochondria were observed under electron microscope. The mitochondrial membrane potential was detected by JC-1.Results: Two groups of aging mice had serious disturbance of estrus cycle. The ovarian area of the mice in the aging non-intervention group was smaller than that in the normal group, and the ovarian area of the mice in the aging intervention group recovered. The ovarian blood flow was weak or even disappear in the aging non-intervention group, and the blood flow in the intervention group was improved. The ovarian volume of mice in the non-intervention group was smaller than that in the normal group. Some ovarian tissues were adhered to the surrounding tissues. While in the intervention group, the ovarian volume increased, the degree of adhesion decreased, the infiltration of ovarian interstitial lymphocytes decreased, and the zona pellucida recovered. Granular cell arrangement returned neatly, egg cell shape recover regular and the number also increased. In the non-intervention group, E2 (Estrogen), AMH (Anti-Mullerian hormone) decreased (P = 0.0092 and P = 0.0334, respectively), FSH (Follicle stimulating hormone) increased (P < 0.0001). In the intervention group, FSH decreased (P = 0.0002), LH (luteinizing hormone) decreased and E2, AMH increased. In the non-intervention group, GSH-Px (Glutathione peroxidase) decreased (P = 0.0129), SOD (Superoxide dismutase) decreased, ROS (reactive oxidative species), MDA (Malondialdehyde) increased. In the aging intervention group, ROS, MDA decreased and GSH-Px increased. In the non-intervention group, mitochondrial expression was scattered at the concentrated distribution point, the length of mitochondria was mostly long and the average volume increased, the density decreased, the number decreased and some mitochondria fused, and lesions such as swelling, vacuolar degeneration and inclusion body formation, membrane potential decreased (P = 0.0002). In the aging intervention group, mitochondria were evenly distributed, the mitochondria were basically round, the distribution density was moderate, the inner ridge was clear, and the membrane potential of the aging intervention group increased.Conclusion: Yu Linzhu can improve the ovarian function of natural aging mice by improving the mitochondrial function of oocytes.
Highlights
Ovarian senescence is a biological process affected by many factors, gradually accumulating and continuously complicated, accompanied by the decrease of mitochondrial number, structural change and productivity of oocytes associated with the decrease of oxidative phosphorylation function
Mitochondrial dysfunction and mitochondrial DNA mutation inhibit the normal development of oocytes
Ovarian senescence is mainly manifested in the decrease of oocyte quantity and quality, accompanied by the decrease of oocyte mitochondrial quantity, structural change and productivity
Summary
Ovarian senescence is a biological process affected by many factors, gradually accumulating and continuously complicated, accompanied by the decrease of mitochondrial number, structural change and productivity of oocytes associated with the decrease of oxidative phosphorylation function. As the most important organelle in the cytoplasm, mitochondria helps oocyte maturation and embryonic development. Mitochondrial dysfunction and mitochondrial DNA mutation inhibit the normal development of oocytes. Mitochondria are the determinants of ovarian senescence [1, 2]. Changes in mitochondrial physiology and metabolism leading to excessive accumulation of reactive oxygen species are considered to be markers of aging [3]. Current studies have shown that age-related changes in mitochondria have a potential impact on oocyte quality in the study of age-related changes in the entire ovarian microenvironment [4]
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