Mechanisms of He Shi Yu Lin formula in treating premature ovarian insufficiency: insights from network pharmacology and animal experiments

This study provides definite evidence for the molecular mechanism by which HSYLF treats POI by decreasing mitochondrial ROS, increasing membrane potential, and improving mitochondrial function. The results from active components of HSYLF and their related key targets also confirmed the characteristics of its multi-component, multi-target, multi-pathway, and overall regulatory effects on POI. Further research regarding the mechanisms is required to generalize these results, and the deeper clinical value of HSYLF also needs to be investigated in the future.