Neobavaisoflavone protects osteoblasts from dexamethasone‐induced oxidative stress by upregulating the CRNDE‐mediated Nrf2/HO‐1 signaling pathway

Abstract

Neobavaisoflavone (NBIF) is a flavonoid, which has a variety of pharmacological activities. However, the mechanism of NBIF in the treatment of osteoporosis still needs further exploration. The differentiation of osteoblast MC‐3T3‐E1 cells after treatment was observed by Alizarin red staining. Cell counting kit‐8 and flow cytometry were used to detect viability, apoptosis, and reactive oxygen species (ROS) levels of treated MC‐3T3‐E1 cells, respectively. Malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) were tested by ELISA kits. The expressions of lncRNA MALAT1, MEG3, CRNDE, Runx2, osteocalcin (OCN), osteopontin (OPN), collagen I (col‐I), nuclear Nrf2, cytoplasm Nrf2, heme oxygenase‐1 (HO‐1) and quinone oxidoreductase 1 (NQO1) in treated MC‐3T3‐E1 cells were examined by Quantitative real‐time PCR or Western blot. Dexamethasone (Dex) inhibited the viability of MC‐3T3‐E1 cells, while the appropriate amount of NBIF had no significantly effect on cell viability. Dex downregulated CRNDE expression, whereas NBIF upregulated CRNDE. Overexpressed CRNDE and NBIF reversed the inhibitory effects of Dex on cell viability, differentiation and levels of SOD, GSH‐Px, Runx2, OCN, OPN, col‐I, nuclear Nrf2, HO‐1 and NQO1 while reversing the promoting effect of Dex on apoptosis and the levels of ROS, MDA, LDH and cytoplasm Nrf2 in MC‐3T3‐E1 cells, respectively, but shCRNDE further reversed the effects of NBIF in MC‐3T3‐E1 cells. NBIF protected osteoblasts from Dex‐induced oxidative stress by upregulating the CRNDE‐mediated Nrf2/HO‐1 signaling pathway.

The Suzuki–Miyaura Cross-Coupling–Claisen Rearrangement–Cross-Metathesis Approach to Prenylated Isoflavones

“…Neobavaisoflavone ( 7 ) was first isolated from the seeds of Psoralea corylifolia , , a plant that is used in traditional Chinese and Indian medicine. Later, it was isolated from root and stem bark of the tree Erythrina sigmoidea in Cameroon. , A wealth of bioactivities have been reported for this natural product, such as antibacterial activity, e.g., against MRSA , or the yeast Zygosaccharomyces parabailii ; the inhibition of DNA polymerase; the stimulation of osteogenesis; the prevention of osteoporosis; or cytotoxicity against human prostate cancer cells . 7-Methoxyneobavaisoflavone ( 9 ) was obtained as a minor component during a phytochemical study on Psoralea corylifolia , and the dimethyl ether 27 was also obtained from neobavaisoflavone ( 7 ) by exhaustive methylation in the course of an isolation study on Erythrina sigmoidea …”

The regulatory activities of MALAT1 in the development of bone and cartilage diseases

“…MALAT1 overexpression or miR-214 inhibition can ameliorate dexamethasone (DEX)-induced inhibition of osteogenic differentiation of BMSCs ( 57 ). The expression of MALAT1 in pre-osteoblast MC3T3-E1 cells can be down regulated by DEX, which has been demonstrated to inhibit osteoblast proliferation and promote osteoblast apoptosis ( 58 ). More specifically, forced expression of MALAT1 can abrogate DEX-induced viability repression and cell apoptosis by suppressing Ppm1e expression and activating AMPK signaling in OB-6 and hFOB1.19 osteoblast cells ( 59 ).…”

A Metal–Organic Framework-Incorporated Hydrogel for Delivery of Immunomodulatory Neobavaisoflavone to Promote Cartilage Regeneration in Osteoarthritis

“…Szliszka et al reported significant inhibition of ROS, reactive nitrogen species (RNS), and the expression of inflammatory cytokines, such as IL-1β, IL-6, IL-12p40, IL-12p70, and TNF-α, in LPS+IFN-γ- or phorbol-12-myristate 13-acetate (PMA)-stimulated RAW264.7 macrophages upon treatment with NBIF. Compounds isolated from Psoralea also stimulate osteogenesis by meditating collagen synthesis to treat bone loss-associated diseases . For example, Xu et al reported that psoralen was shown to work on cartilages, and it promoted cartilaginous gene expressions (e.g., type II collagen, aggrecan, and SOX-9) in rat chondrocytes.…”