Protective Mechanism of Luteinizing Hormone and Follicle-Stimulating Hormone Against Nicotine-Induced Damage of Mouse Early Folliculogenesis

Abstract

Previous studies have shown that nicotine could impair the germ cell cyst breakdown and the primordial follicle assembly by autophagy. In this paper, we discovered that luteinizing hormone (LH) and follicle-stimulating hormone (FSH) could counteract the damage caused by nicotine of mouse germ cell cyst breakdown. The neonatal mice were separately intraperitoneally injected with nicotine, nicotine plus LH, nicotine plus FSH, and saline (control) for 4 days. Compared with the nicotine group, the quality of oocytes and the number of follicles were remarkably increased in the nicotine plus LH group or nicotine plus FSH group. LH and FSH could alleviate nicotine-induced oocyte autophagy by different pathways. LH reduced the nicotine-induced autophagy by restoring the phosphorylation level of adenosine 5′-monophosphate-activated protein kinase α-1, while FSH by downregulating the phosphorylation level of Forkhead box class O 1. In addition, in a subsequent study of 6-week mice in different treated groups, we found that LH and FSH supplementation significantly improved normal maturation rates, fertilization rates, and embryo’s developmental potential of oocytes in oocytes exposed to nicotine. Taken together, these results suggested that LH and FSH could counteract the damage caused by nicotine and finally ensure normal germ cell cyst breakdown and early embryo development.

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“…LH reduces nicotine-induced autophagy by restoring the phosphorylation of adenosine 5'-monophosphate-activated protein kinase α-1. By contrast, FSH reduces autophagy by downregulating the phosphorylation of forkhead box O1 (FoxO1) and light chain 3 (LC3)-II (112,113). Paradoxically, FSH upregulates Beclin1 through the PI3K/JNK/c-Jun pathway to accelerate the degradation of lipid droplets in mammalian follicular granulosa cells, thus enhancing autophagy.…”

“…Paradoxically, FSH upregulates Beclin1 through the PI3K/JNK/c-Jun pathway to accelerate the degradation of lipid droplets in mammalian follicular granulosa cells, thus enhancing autophagy. FSH affects follicular development, and participates in the regulation of lipid metabolism (such as cholesterol and fat), regulates bone density, and is associated with the onset of cardiovascular diseases, and the occurrence of breast cancer (112). FSH activates liver cholesterol biosynthesis and decreases serum cholesterol through the Gi2α/β-inhibin-2/Akt pathway during menopause (114).…”