Kaempferol Alleviates Mitochondrial Damage by Reducing Mitochondrial Reactive Oxygen Species Production in Lipopolysaccharide-Induced Prostate Organoids.

Common prostate diseases such as prostatitis and benign prostatic hyperplasia (BPH) have a high incidence at any age. Cellular stresses, such as reactive oxygen species (ROS) and chronic inflammation, are implicated in prostate enlargement and cancer progression and development. Kaempferol is a flavonoid found in abundance in various plants, including broccoli and spinach, and has been reported to exhibit positive biological activities, such as antioxidant and anti-inflammatory properties. In the present study, we introduced prostate organoids to investigate the protective effects of kaempferol against various cellular stresses. The levels of COX-2, iNOS, p-IκB, a pro-inflammatory cytokine, and ROS were increased by LPS treatment but reversed by kaempferol treatment. Kaempferol activated the nuclear factor erythroid 2-related factor 2(Nrf2)-related pathway and enhanced the mitochondrial quality control proteins PGC-1α, PINK1, Parkin, and Beclin. The increase in mitochondrial ROS and oxygen consumption induced by LPS was stabilized by kaempferol treatment. First, our study used prostate organoids as a novel evaluation platform. Secondly, it was demonstrated that kaempferol could alleviate the mitochondrial damage in LPS-induced induced prostate organoids by reducing the production of mitochondrial ROS.

Pueraria montana var. lobata root extract inhibits photoaging on skin through Nrf2 pathway.

Pueraria montana var. lobata is a bioactive substance, in possession of a variety of beneficial health effects, which has long been extensively used as a traditional medication for the treatment of fever, acute dysentery, diabetes, and cardiovascular diseases in North-East Asian countries. The purpose of this study was to evaluate the cytoprotective activity of Pueraria montana var. lobata ethanol extract (PLE) for ultraviolet B (UVB) induced oxidative stress in human dermal fibroblasts (HDF). It was hypothesized that PLE treatment (25-100 µg/mL) would reduce intracellular reactive oxygen species (ROS) levels as well as increase collagen production in UVB-irradiated HDF. The results confirmed this theory, with collagen production increasing in the PLE treatment group in a dose-dependent manner. In addition, regulators of cellular ROS accumulation, including HO-1 and NOQ-1, were activated by Nrf2, which was mediated by PLE. Hence, intracellular levels of ROS were also reduced in the PLE treatment group in a dose-dependent manner. In conclusion, PLE increases collagen production and maintains hyaluronic acid (HA) levels in human dermal fibroblasts exposed to UVB-irradiation, thereby inhibiting photoaging.