The inhibition of PSII activity observed with nonphysiological doses of Spm or Spd was considered harmful when the activity of PSII was studied separately in isolated thylakoids or PSII submembrane fractions. But, in vivo, when PSII pumps electrons to the PSI complex under stress conditions, the importance of PSII deactivation must be taken into account. Especially, when the PSII repair and PAs biosynthesis are finely controlled and require PSI activity to fulfill the need for ATP. This point of view is important in the understanding of the importance of PSI resistance to photoinhibition in vivo. Osteoporosis is a major health problem among the elderly and is characterized by low bone mineral density and microarchitectural deterioration of bone, leading to increased fracture risks. Osteoporosis is prevalent among women, in particular postmenopausal women. Ruxolitinib Estrogen shortage/deficiency results in an increase in bone turnover, wherein the rate of osteoclastic resorption exceeds the rate of osteoblastic osteogenesis, leading to a net loss of bone mass. Many studies have indicated that hormone replacement therapies can be used to prevent and/or treat postmenopausal osteoporosis. However, long-term estrogen supplementation poses several risks, e.g., endometrial cancer, breast cancer, ovarian cancer, and cardiovascular diseases, and is no longer recommended. Previous studies suggest that estrogen may inhibit osteoclast activity through regulating the levels of serum CT and PTH. Estrogen stimulates the synthesis of CT, which directly inhibits osteoclast differentiation and activity, and thus reduces the number of osteoclasts and serum concentration of Ca2+. PTH is one of the most important peptide hormones that regulate calcium and phosphorus homeostasis and bone remodeling. Estrogen can decrease the expression of PTH and lead to a decrease in serum levels of PTH. Estrogen also inhibits PTHstimulated adenylate cyclase activity and thus PTH-stimulated bone resorption. In addition, estrogen shortage has been found to increase serum levels of BGP in postmenopausal women. BGP, also known as c-carboxyglutamic acid protein, is a hormone-like peptide synthesized and secreted by osteoblasts. BGP is not only an indicator of in vivo bone formation rate but also a positive regulator of bone mineralization. In addition to these hormones, estrogen inhibits bone resorption by suppressing secretion of key osteolytic cytokines such as IL-1 and IL-6 by bone marrow stromal cells and osteoblasts. These cytokines are positive regulators of osteoclast activity and bone resorption. Besides, these cytokines may crosstalk with each other to synergistically promote osteoclastogenesis and bone resorption. For example, IL-1, including both IL-1a and IL-1b subunits, can induce osteoblasts to secrete IL-6 to further promote bone resorption. Estrogen, IL-1b, and IL-6 also regulate PGE production, which promotes proliferation and differentiation of osteoclast precursors. Previous studies have reported that PGE2 could also stimulate bone resorption by increasing IL-6 transcription. Furthermore, IL-1 was found to increase COX-2 expression at the mRNA and protein levels, leading to an increase in prostaglandin production. The stabilization of COX-2 mRNA is the most important basis of continued increase in COX-2 protein.