Serenoa repens extracts promote hair regeneration and repair of hair loss mouse models by activating TGF-ß and mitochondrial signaling pathway.

OBJECTIVE: Plenty of plant extracts have been used for treating hair loss. This study aims to investigate the effects of liposterolic extracts of Serenoa repens (LSESr) on hair cell growth and regeneration of hair, and clarify the associated mechanisms. MATERIALS AND METHODS: Human keratinocyte cells (HACAT) were cultured, incubated with dihydrotestosterone (DHT) and treated with LSESr. Cell viability was examined by using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H- tetrazolium bromide (MTT) assay. Hair loss C57BL/6 mouse model was established by inducing with DHT. Hair growth, density, and thickness were evaluated. Back skin samples were collected and stained with hematoxylin and eosin (HE) assay. B-cell lymphoma-2 (Bcl-2), Bcl-2 associated protein X (Bax), cleaved caspase 3 and transforming growth factor ß2 (TGF-ß2) were examined using Western blot assay. RESULTS: LSESr treatment significantly increased HACAT cell viabilities compared to DHT-only treated cells (p<0.05). LSESr treatment post injection of DHT significantly converted skin color from pink to gray and increased hair density, weight and thickness compared to DHT-only treated mice (p<0.05). LSESr treatment significantly triggered follicle growth and decreased inflammatory response. LSESr treatment significantly decreased TGF-ß2 and cleaved caspase 3 expression of hair loss mouse models compared to that of DHT treated mice (p<0.05). LSESr treatment significantly enhanced Bcl-2 expression and reduced Bax expression compared to that of DHT treated mice (p<0.05). Meanwhile, effects of LSESr were substantial even achieving to the potential of finasteride. CONCLUSIONS: LSESr promoted the hair regeneration and repair of hair loss mouse models by activating TGF-ß signaling and mitochondrial signaling pathway.

Protective effect of nimodipine against cerebral injury induced by subacute carbon monoxide intoxication in mice.

AIM: To study the effects of nimodipine on delayed cerebral injury in mice from subacute carbon monoxide (CO) exposure. METHODS: Mice were exposed to CO (100 mL/kg, ip) once a day, continuously for 7 d. After 7-d CO-exposure, mortality in mice, changes in learning ability and memory using passive avoidance test, the pathomorphologic observation of brain tissue slices, and changes of monoamine oxide (MAO)-B activities in cerebral tissue were studied. Nimodipine was administered 30 min before CO-exposure every time. RESULTS: The preadministration of nimodipine decreased the mortality in mice, almost reversed the impairment of learning and memory function, prevented the hippocampal neurons against delayed death and blunted the rise of MAO-B activity after subacute CO poisoning of mice. CONCLUSION: Pretreatment with nimodipine markedly prevented mice from delayed encephalopathy after CO poisoning.

Experimental and clinical investigation on oxiconazole.

A new antimycotic imicazole drug, oxiconazole, used both in vitro and in vivo in the treatment of 212 cases of tinea corporis, tinea cruris and tinea pedis is reported. In vitro, it shows marked antimycotic effect against 24 strains of pathogenic fungi except those of Wangiella dermatitides and 3 strains of Aspergilli. The minimal inhibition concentration (MIC) to Epidermophyton floccosum and Candida guilliermondi are 1 microgram/ml and 0.5 microgram/ml. The cure rate of 2% cream of oxiconazole in 124 cases of tinea corporis and tinea cruris is 90.3%, and in 88 cases of tinea pedis, 89.78%.