RESUMO
The anti-inflammatory and anti-oxidant effect of equine placental extract (ePE) on epidermal keratinocytes was examined. ePE reduced mRNA levels of TNF-α (Tumor Necrosis Factor-α) and IL-6 (Interleukin-6) among the inflammatory cytokines released by epidermal keratinocytes after ultraviolet light (UVB: 290-320 nm) exposure. ePE also activated Nrf2, a transcription factor known to be activated by oxidative stress to promote the expression of antioxidant enzymes and suppress inflammation, and it increased the mRNA level of the antioxidant enzyme HO-1 (Heme Oxygenase-1). These results suggest that ePE suppresses UV-induced inflammation of epidermal keratinocytes via activation of Nrf2.
RESUMO
Improvement of hair thinning was observed after a novel treatment course involving basalt stone and placental extract application in a patient of androgenetic alopecia. The patient was resistant to the general home care treatment. The response to the new treatment may be attributed to the decreased scalp hardness secondary to the improved blood circulation after basalt stone massage and the hair growth-promoting action of the placental extract. Furthermore, recurrence of hair thinning was observed after suspension of this treatment; however, this hair thinning improved when the treatment was resumed.
RESUMO
In the present study, we assessed the antiaging effect of equine placental extract (ePE) on dermal fibroblasts and found that it markedly suppressed the appearance of β-galactosidase-positive cells among the senescent cells induced by repeated hydrogen peroxide exposure or ultraviolet A irradiation. Moreover, the efficacy of ePE treatment was similar to that of an antioxidant, N-acetylcysteine. Thus, owing to its antioxidant effect, ePE can be used as an antiaging agent, particularly for the dermis.
RESUMO
Objectives: To analyze the effect of human placental extracts (HPEx) on hepatocellular carcinoma cells in vitro. Methods: The hepatocellular carcinoma cell lines, namely, HLE and Huh-7, were used. The cells were subjected to a growth assay using the formazan dye method; the effect of combination treatment with sorafenib and HPEx was also assessed. The preventing normal cell damage effect of HPEx was analyzed by virtual therapy where possible; the experimental protocol was constructed on the basis of pre- and post-sorafenib treatment data. Cytotoxicity was measured by lactate dehydrogenase (LDH) assay. Results: HPEx caused significant dose-dependent suppression in the growth of HLE and Huh-7 cells. These tumor cells were significantly suppressed by combination treatment with HPEx and sorafenib. In addition, HPEx potentiated sorafenib sensitivity against tumor cells, and significantly prevented sorafenib-induced cytotoxicity in primary cultured rat hepatocytes under all designed experimental conditions. Specifically, pre-treatment with HPEx had a greater effect than post-treatment with HPEx. Conclusion: HPEx suppresses tumor cell growth, potentiates sorafenib efficacy, and has a preventing normal cell damage effect; this triple functionality of HPEx makes it a useful agent for liver cancer therapy.