Tripterine Inhibits Proliferation and Promotes Apoptosis of Keloid Fibroblasts by Targeting ROS/JNK Signaling.

Keloids are benign skin tumors characterized by excessive fibroblast proliferation and collagen deposition. The current treatment of keloids with hormone drug injection, surgical excision, radiotherapy, physical compression, laser therapy, cryotherapy often have unsatisfactory outcomes. The phytochemical compounds have shown great potential in treating keloids. Tripterine, a natural triterpene derived from the traditional Chinese medicine Thunder God Vine (Tripterygium wilfordii), was previously reported to exhibit an anti-scarring bioactivity in mouse embryonic fibroblast NIH/3T3 cells. Accordingly, our study was dedicated to explore its role in regulating the pathological phenotypes of keloid fibroblasts. Human keloid fibroblasts were treated with tripterine (0-10 µM) for 24 hours. Cell viability, proliferation, migration, apoptosis, and extracellular matrix (ECM) deposition were determined by CCK-8, EdU, wound healing, Transwell, flow cytometry, western blotting, and RT-qPCR assays. The effects of tripterine treatment on reactive oxygen species (ROS) generation and JNK activation in keloid fibroblasts were assessed by DCFH-DA staining and western blotting analysis. Tripterine at the concentrations higher than 4 µM attenuated the viability of human keloid fibroblasts in a dose-dependent manner. Treatment with tripterine (4, 6, and 8 µM) dose-dependently inhibited cell proliferation and migration, promoted cell apoptosis, reduced α-SMA, Col1, and Fn expression, induced ROS production, and enhanced JNK phosphorylation in keloid fibroblasts. Collectively, tripterine ameliorates the pathological characteristics of keloid fibroblasts that are associated with keloidformation and growth by inducing ROS generation and activating JNK signalingpathway.

Protective effects of Dendrobium candidum Wall ex Lindl. on high-fat diet-induced liver damage in mice.

D. candidum Wall. ex Lindl. (D. candidum) is a traditional Chinese herbal medicine with multiple therapeutic properties. D. candidum was administered to mice with high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) and its mechanism of action was elucidated. D. candidum was intragastrically administered to HFD mice for 6 weeks at a dosage of 200 or 400 mg/kg. D. candidum reduced body weight gain and blood glucose levels in HFD mice in a dose-dependent manner, while significantly reducing lipid accumulation in the liver. D. candidum significantly regulated the expression of lipid metabolism- and gluconeogenesis-related genes and inhibited activation of the NLRP3 inflammasome. In summary, D. candidum significantly inhibits fat accumulation, maintains lipid metabolism and glucose homeostasis, and inhibits the inflammatory response in the liver of HFD mice. Our findings suggest that D. candidum may be an effective therapeutic strategy against NAFLD injury. PRACTICAL APPLICATIONS: The occurrence and development of fatty liver is closely related to abnormalities in lipid and glucose metabolism. An HFD-induced NAFLD mouse model was used to study the effects of D. candidum. After treatment with D. candidum, lipid and glucose metabolism in the mice was effectively regulated, which reduced liver damage and fat storage with obvious protective effects on the liver. Our results suggest that D. candidum has potential for further clinical application in the treatment of NAFLD.