Salvianolic acid-A alleviates oxidative stress-induced osteoporosis.

AIM: Cellular damage induced by oxidative stress contributes to systemic bone disorders leading to osteoporosis. Bone homeostasis regulates the balance between the functions of osteoblasts and osteoclasts. Osteoblast cells are responsible for bone formation and are very sensitive to oxidative stress. Polyphenolic compounds possess the ability to scavenge free radicals, thus reducing intracellular oxidative stress. Natural compounds such as salvianolic acid A (SAL-A) exhibit prominent antioxidant properties. However, its antioxidant role in bone homeostasis is poorly defined. In this study, we aimed to elucidate the potential role of SAL-A in protecting the osteoblasts from H2O2-induced oxidative stress.

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METHODS

Rat osteoblast cells were treated with or without 500 μM H2O2 in the presence or absence of 5 μM and 10 μM of SAL-A. A series of assays such as cell viability by CCK-8 kit, detection of reactive oxygen species by dichlorodihydrofluorescein diacetate (DCFH-DA), mitochondrial membrane potential by JC-1 fluorescence, level of bone mineralization proteins osteocalcin, bone sialoprotein, and alkaline phosphatase by immunocytochemistry studies, were conducted.

KEY FINDINGS: SAL-A protected the rat osteoblast cells from H2O2-induced cytotoxicity by significantly attenuating free radical generation, thus improving cell viability. SAL-A treatment also significantly restored bone mineralization proteins, including osteocalcin, bone sialoprotein, and alkaline phosphatase, which were aggravated by H2O2-induced oxidative stress.

SIGNIFICANCE: The study results provide the role of SAL-A in protecting the osteoblasts from H2O2-induced oxidative stress in rat osteoblast cells by scavenging the free radicals, increasing the cell viability, mineralization, and differentiation of osteoblasts.