α-Bisabolol suppresses the inflammatory response and ECM catabolism in advanced glycation end products-treated chondrocytes and attenuates murine osteoarthritis.

As a chronic musculoskeletal degeneration disease, osteoarthritis (OA) clinically manifests as joint pain, stiffness and a limited range of movement. OA has affected the life quality of at least one-tenth of the population but lacks satisfactory treatments. α-Bisabolol (BISA) is a small oily sesquiterpene alcohol widely found in essential oils of chamomile (Matricaria recutita), salvia and wood of Candeia and has multiple biological properties, particularly an anti-inflammatory effect. The purpose of this study is to assess the anti-inflammatory and chondroprotective effect of BISA in OA progression and explore its underlying mechanism. We isolated human chondrocytes and treated them with advanced glycation end products (AGEs) to imitate OA progression in vitro. BISA pretreatment suppressed the AGE-induced inflammatory reaction and extracellular matrix (ECM) degeneration by blocking nuclear factor kappa B (NF-κB), p38 and c-Jun N-terminal kinase (JNK) signaling. Moreover, a mouse destabilization of the medial meniscus (DMM) model was established by surgery to investigate BISA protection in vivo. BISA administration attenuated DMM-induced radiological and histopathological changes relative to the DMM group and resulted in lower OARSI scores. Taken together, the results of our study indicate the potential of BISA in OA therapy.

Effects of Rhizoma Drynariae Cataplasm on Fracture Healing in a Rat Model of Osteoporosis.

BACKGROUND Osteoporosis is an increasingly prevalent disease characterized by decreased bone mass and deterioration of the bone microstructure, which contribute to increased fragility and subsequent fragility fractures, especially in elderly individuals. Rhizoma Drynariae (DRE) is among the most frequently used herbal medicines for the treatment of osteoporosis. Transdermal delivery is a proven novel pathway for drug treatment and has several advantages over traditional drug delivery routes. MATERIAL AND METHODS Female Sprague-Dawley osteoporotic fracture model rats were divided into 3 groups: the control group, the DRE (90 mg/kg/day) group and the DRE cataplasm (containing 30 mg DRE, administered at right femur site daily) group. At 3 and 6 weeks after operation, we performed x-ray, histological, and biomechanical analyses, and evaluated bone marrow density of the femur. RESULTS Treatment with DRE increased callus formation and bone union compared with the control group. Moreover, DRE enhanced bone strength at the femoral diaphysis in the osteoporotic fractures in rats by increasing the ultimate load and stiffness compared with the control group. Furthermore, DRE restored the trabecular bone mineral density in the femur compared with the control group. DRE cataplasm application further enhanced the therapeutic effects against osteoporotic fracture in this rat model. CONCLUSIONS DRE cataplasm application might be useful against osteoporotic fracture.

Panax quinquefolius saponin inhibits endoplasmic reticulum stress-mediated apoptosis and neurite injury and improves functional recovery in a rat spinal cord injury model.

The treatment goal in spinal cord injury (SCI) is to repair neurites and suppress cell apoptosis. Panax quinquefolius saponin (PQS) is the major active ingredient of American ginseng and has been demonstrated to have anti-inflammatory and anti-apoptotic roles in various diseases. However, the potential effect of PQS on the pathological process of acute SCI remains unknown. This work tested the effects of PQS on acute SCI and clarified its potential mechanisms. PQS treatment ameliorated the damage to spinal tissue and improved the functional recovery after SCI. PQS treatment inhibited endoplasmic reticulum (ER) stress and the associated apoptosis after acute SCI. PQS further abolished the triglyceride (TG)-induced ER stress and associated apoptosis in neuronal cultures. PQS appears to inhibit the ER-stress-induced neurite injury in PC12 cells. Our results suggest that PQS is a novel therapeutic agent for acute central nervous system injury.