Andrographolide reversed TGF-β1-induced fibrogenesis, restored glutathione levels, and suppressed reactive oxygen species accumulation in human lung fibroblasts.
Andrographolide exerts antifibrotic effects in human lung fibroblasts by restoring glutathione metabolism and suppressing reactive oxygen species accumulation.
Pulmonary fibrosis is a progressive lung disorder characterized by fibroblast activation and excessive extracellular matrix deposition. Andrographolide (ANDRO) has been reported to attenuate pulmonary fibrosis, but the underlying molecular mechanisms remain incompletely understood. In this study, we investigated the effects of ANDRO on transforming growth factor-beta 1 (TGF-β1)-induced fibrogenesis in human lung fibroblasts. Comprehensive transcriptomic analysis revealed that ANDRO reversed TGF-β1-perturbed genes associated with fibrogenesis and glutathione (GSH) metabolism. Functionally, ANDRO restored TGF-β1-inhibited total GSH levels and suppressed TGF-β1-induced reactive oxygen species (ROS) accumulation. Together, these findings identify GSH metabolism as a previously unrecognized mechanism underlying the antifibrotic effects of ANDRO in human lung fibroblasts.
Tseng et al. (Wed,) conducted a other in Pulmonary fibrosis. Andrographolide (ANDRO) vs. TGF-β1 was evaluated on Fibrogenesis, glutathione (GSH) metabolism, and reactive oxygen species (ROS) accumulation. Andrographolide reversed TGF-β1-induced fibrogenesis, restored glutathione levels, and suppressed reactive oxygen species accumulation in human lung fibroblasts.