Cinnamtannin B-1 Prevents Ovariectomy-Induced Osteoporosis via Attenuating Osteoclastogenesis and ROS Generation

Abstract

Osteoporosis (OP) is one of the common bone metabolic diseases that endangers postmenopausal women and the elders. Both excessive bone resorption caused by osteoclast over-activation and increased oxidative stress are associated with osteoporosis. Cinnamtannin B-1 (CB-1) is considered as a high-valued plant extract monomer due to its antioxidant properties. However, the mechanism of CB-1 impacts on reducing oxidative stress, inhibiting the production of reactive oxygen species (ROS) and osteoclast differentiation and preventing ovariectomy-induced osteoporosis are still unclear. In this study, the effects of CB-1 on nuclear factor κB (RANKL)-induced osteoclasts formation and differentiation in vitro and the potential therapeutic effect on ovariectomy (OVX)-induced osteoporosis in vivo are investigated. CB-1 was found to inhibit osteoclast formation and bone resorption function in a dose-dependent manner, and it inhibited specific genes related to osteoclast as well. Micro-CT and histopathological staining showed that CB-1 can effectively prevent OVX-induced osteoporosis. In addition, CB-1 treatment can effectively inhibit the production of reactive oxygen species (ROS) in vivo and in vitro . Mechanistically, CB-1 inhibits the activation of osteoclasts by inhibiting the activation of the NF-κB signaling pathway. In conclusion, CB-1 would be able to be used as a promising new drug strategy to inhibit RANKL-induced osteoclastogenesis and prevent ovariectomy-induced osteoporosis.

Inhibition of lytic polysaccharide monooxygenase by natural plant extracts

“…Cinnamtannin isomers have been reported in various Cinnamomum species, as well as a number of other plant species (Virtbauer et al ., 2008; Idowu et al ., 2010; Wen et al ., 2015; González De Llano et al ., 2019; Li et al ., 2020; Maeda, 2020; Yang et al ., 2020). This further strengthens the expectation that plants may contain compounds with cellulolytic‐enzyme‐modulating properties, and that proanthocyanidins, such as cinnamtannin, may play a role in LPMO inhibition.…”

Effect of The Autophagy Mechanism of TSCs Induced by Oxidative Stress Under Beclin1-mTOR Interaction

“…Current theories indicate that a small number of resident stem cells maintain the maintenance and repair of adult tissues [8]. Recently, tendon-derived stem cells (TSCs) from human, mouse and rat tendon tissues have been identi ed [9,10]. Unlike static tendon cells, TSCs have the potential for multiple differentiation and self-renewal, and are the core of tendinopathy's occurrence, development and healing.…”

“…It has a regulatory effect on mammalian bone development, bone formation, bone remodeling, and blood vessel formation. It is clearly a rmed [9] that local osteogenesis and angiogenesis have always been regarded as the important basis of tendon bone healing process. Beclin1 is a key regulator of autophagy and an indispensable condition for the formation of autophagosomes.…”

Integration of Proteomics and Metabonomics in Exploring the Protecting Mechanism of Gushukang Capsule in Osteoporosis Rats

“…Its function is related to the scavenging of reactive oxygen species [30]. In postmenopausal women, the level of estrogen and antioxidants decreased with age, and the ROS accumulated in the body could not be cleared in time, which induced the occurrence of oxidative stress and led to the damage of osteoblasts and osteocytes [31,32]. ALDH can reduce oxidative stress through a variety of aldehyde metabolism [33].…”