Parthenolide is a natural product from the shoots of Tanacetum parthenium that has been demonstrated to have immunomodulatory effects in a number of diseases. The present study aimed to determine the effect and mechanism of parthenolide on the apoptotic ability of H2O2‑induced osteoblasts. Cell viability was analyzed with a MTT assay and the apoptotic rate was subsequently measured using flow cytometry. The activity of the antioxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX), and the serum marker enzymes alkaline phosphatase (ALP), malondialdehyde (MDA) and lactate dehydrogenase (LDH) was measured. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses were performed to analyze the expression levels of osteogenesis and oxidative stress‑associated genes. The results indicated that parthenolide increased cell viability and inhibited the apoptosis of H2O2‑induced osteoblasts. Parthenolide decreased the levels of reactive oxygen species, MDA, LDH and ALP. SOD and GPX levels were increased by parthenolide in H2O2‑induced osteoblasts. This suggested that parthenolide may break the equilibrium state of oxidative stress and inhibit cellular apoptosis. Parthenolide additionally increased the expression levels of oxidative stress‑associated genes, including nuclear factor erythroid 2 like 2, hemeoxygenase‑1 and quinone oxidoreductase 1 in H2O2‑induced osteoblasts. Furthermore, parthenolide increased the expression of osteogenesis‑associated genes, including runt‑related transcription factor 2, osteopontin, osteocalcin and collagen 1 in H2O2‑inducedosteoblasts. Therefore, it was concluded that parthenolide may be used in the treatment of osteoporosis.

Introduction: Oxidative stress is the main cause of osteoarthritis (OA). Lycium barbarum polysaccharides (LBP) have antioxidant properties. Thus, the potential effect of LBP on H 2 O 2-stimulated chondrocytes was examined. Material and methods: The cell viability was detected by CCK-8. The reactive oxygen species (ROS) production and apoptosis rates were determined by flow cytometric analysis. The DNA damage was detected by comet assay. Real-time polymerase chain reaction (qPCR) and Western blot assays were performed to examine the expression of histone 2A family member X (γH2AX), checkpoint kinase 1 (Chk1), poly ADP-ribose polymerase (PARP), cysteinyl aspartate specific proteinase (caspase)-3/8/9, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and its antioxidant-response element (ARE) dependent factors including heme oxygenase-1 (HO-1) and quinine oxidoreductase-1 (NQO-1). Results: Compared to the H 2 O 2 group, LBP inhibited the ROS production and DNA damage caused by H 2 O 2 (p < 0.05), respectively. LBP inhibited the mRNA and protein expressions of γH2AX and Chk1 (p < 0.05). Meanwhile, LBP significantly decreased apoptosis (p < 0.05). And LBP inhibited the expression levels of PARP and Caspase-3/8/9 (p < 0.05). Moreover, LBP increased the expression of Nrf2, HO-1and NQO-1 (p < 0.05). Furthermore, the depletion of Nrf2 that mediated by RNA interference reversed the apoptosis and DNA damage inhibition effect of LBP (p < 0.05). Conclusions: LBP protected chondrocytes through inhibiting DNA damage and apoptosis caused by H 2 O 2 , in which the Nrf2/ARE signaling pathway played a positive role. It provided an inspiration for clinical applicationdeveloping LBP as a therapeutic agent and Nrf2 as a promising candidate.