Ultraviolet (UV) irradiation is a crucial factor that leads to skin photoaging and results in increased DNA damage, oxidative stress, and collagen degradation. Jasmine flowers have been utilized as a traditional medicine in Asia to treat various diseases, including dermatitis, diarrhea, and fever. Furthermore, the fermented broth of Lactobacillus rhamnosus has been reported to exert protective effects on the skin. In the present study, jasmine flower extract was fermented with L. rhamnosus. We investigated the antioxidant and collagen‐promoting effects on UVB/H2O2‐induced HS68 dermal fibroblast cell damage. The results indicated that treatment with the fermented flower extracts of Jasminum sambac (F‐FEJS) could enhance the viability of HS68 cells. Furthermore, the UVB/H2O2‐induced excessive production of reactive oxygen species, degradation of collagen, activation of MAPKs, including P38, ERK, and JNK, and premature senescence were remarkably attenuated by F‐FEJS in dermal fibroblast cells. The nuclear accumulation of p‐c‐jun, which is downstream of MAPK, and the inactivation of p‐smad2/3, which is one of the crucial transcription factors that enhance collagen synthesis, were reversed in response to F‐FEJS treatment in UVB/H2O2‐exposed cells. Notably, the expression of antioxidant genes, such as HO‐1, and the nuclear translocation of Nrf2 were further enhanced by F‐FEJS in UVB/H2O2‐treated cells. Interestingly, the F‐FEJS‐induced increase in ARE luciferase activity indicated the activation of Nrf2/ARE signaling. In conclusion, our findings demonstrated that F‐FEJS can effectively ameliorate UVB/H2O2‐induced dermal cell aging and may be considered a promising ingredient in skin aging therapy.

Skin pigmentation is resulted from several processes, such as melanin synthesis transportation and abnormal melanin accumulation in keratinocytes. Various studies have suggested that seven traditional Chinese herbal extracts from Atractylodes macrocephala, Paeonia lactiflora, Bletilla striata, Poria cocos, Dictamnus dasycarpus, Ampelopsis japonica and Tribulus terrestris (which we collectively named ChiBai), show several protective effects toward skin‐related diseases. Lactobacillus rhamnosus, a lactic acid bacterium, has been reported to treat skin inflammation and atopic dermatitis. In this study, the broth produced by the cofermentation of ChiBai with Lactobacillus rhamnosus was studied for its effects on skin pigmentation through in vitro and in vitro experiments. In the in vitro experiments, we found that the fermented broth of ChiBai (FB‐ChiBai) suppressed alpha‐melanocyte stimulating hormone (α‐MSH)‐induced melanogenesis in B16F0 murine melanoma cells without any cytotoxicity at a concentration of 0.5%. FB‐ChiBai significantly attenuated melanin production, tyrosinase activities and melanogenesis‐related signaling pathways. Treatment with FB‐ChiBai also reduced the nuclear translocation and promoter binding activities of MITF. In the in vivo experiments, FB‐ChiBai was topically applied to the dorsal skin of C57BL/6J nude mice and concurrently irradiated with UVB, three times a week for 8 weeks. The results indicated that FB‐ChiBai alleviated UVB‐induced hyperpigmentation by reducing epidermal hyperplasia and inhibiting the CREB/MITF/tyrosinase pathway. In conclusion, our data indicated that the anti‐melanogenic effects of FB‐ChiBai are mediated by the inhibition of CREB/MITF/tyrosinase signaling pathway. The findings suggest that FB‐ChiBai can protect against UV‐B irradiation and that it might be used as an agent in cosmetic products to protect against UVB‐induced hyperpigmentation.

Nonalcoholic fatty liver disease (NAFLD) is considered to be a serious clinical complication, which could cause significant liver dysfunction including fibrosis, cirrhosis, and cancer. Obesity could lead to NAFLD and contributes to liver disorder and related complicated liver diseases. Effect of exercise combined with alcalase treatment derived potato protein hydrolysate (APPH) on high-fat diet (HFD)-induced hepatic injury was investigated in senescence accelerated mouse-prone 8 (SAMP8) mice in the present study. Mice were divided into six groups (n = 6): Group I-Control, Group II-HFD, Group III-Exercise, Group IV-HFD + APPH, Group V-HFD + Exercise, and Group VI-HFD + Exercise + APPH. Combined APPH treatment and exercise offer better cytoprotection in HFD-induced histological changes than APPH treatment and exercise alone. Further, APPH and exercise activate the cell survival proteins PI3K/Akt and prevent FasL/FADD-mediated apoptosis in HFD fed SAMP8 mouse. APPH with swimming exercise effectively modulate HFD-induced liver damage and apoptosis in aged mice through activation of PI3K/Akt protein. How to cite this article: Chuang H-L, Baskaran R, Hsuan Day C, et al. Role of potato protein hydrolysate and exercise in preventing high-fat diet-induced hepatocyte apoptosis in senescence-accelerated mouse.

Epimedium, is used traditionally in Chinese medicine to treat infertility problems. In this study, we establish the cell model to elucidate the protective effect of epimedium against ES by analyzing the molecular relationship between mitochondrial dynamics and steroidogenesis and to explore the molecular mechanism focusing on mitochondria function relating to fertility. ES induced ROS accumulation in mitochondria and the epimedium treatment significantly reduced the ROS accumulation. Furthermore, mitochondria morphology was restored to elongated shape following epimedium treatment. Epimedium treatment promoted dynamin‐associated protein 1 (Drp1)‐mediated steroidogenesis pathway by upregulating PKA, CREB, Drp1, and StAR protein expression in response to ES exposure in Leydig cells. Moreover, it was also identified that, CREB plays an important role in epimedium activation in Drp1‐mediated steroidogenesis signaling pathway by increasing, phospho‐CREB expression in nucleus. Testosterone level is decreased in ES‐exposed cells; however, the testosterone level was increased after epimedium treatment. In conclusion, epimedium treatment improved mitochondria function in ES‐exposed Leydig cells and activated downstream Drp1‐dependent steroidogenesis by CREB mediated signaling pathway.

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