Baicalin is a traditional Chinese herbal medicine commonly used for hair loss, the precise molecular mechanism of which is unknown. In the present study, the mechanism of baicalin was investigated via the topical application of baicalin to reconstituted hair follicles on mice dorsa and evaluating the effect on canonical Wnt/β-catenin signaling in the hair follicles and the activity of dermal papillar cells. The results indicate that baicalin stimulates the expression of Wnt3a, Wnt5a, frizzled 7 and disheveled 2 whilst inhibiting the Axin/casein kinase 1α/adenomatous polyposis coli/glycogen synthase kinase 3β degradation complex, leading to accumulation of β-catenin and activation of Wnt/β-catenin signaling. In addition, baicalin was observed to increase the alkaline phosphatase levels in dermal papillar cells, a process which was dependent on Wnt pathway activation. Given its non-toxicity and ease of topical application, baicalin represents a promising treatment for alopecia and other forms of hair loss. Further studies of baicalin using human hair follicle transplants are warranted in preparation for future clinical use.
The distinct time-phases of Ca influx in MCs induced by UVA or UVB contribute to the consecutive stimulation of melanosome transfer, thereby providing a potent photoprotection against harmful UV radiation.
Fungal entomopathogens are largely facultative parasites and play an important role in controlling the density of insect populations in nature. A few species of these fungi have been used for biocontrol of insect pests. The pattern of the entomopathogen competition for insect individuals is still elusive. Here, we report the empirical competition for hosts or niches between the inter- and intra-species of the entomopathogens Metarhizium robertsii and Beauveria bassiana. It was found that the synergistic effect of coinfection on virulence increase was not evident, and the insects were largely killed and mycosed by M. robertsii independent of its initial co-inoculation dosage and infection order. For example, >90% dead insects were mycosed by M. robertsii even after immersion in a spore suspension with a mixture ratio of 9:1 for B. bassiana versus M. robertsii. The results thus support the pattern of competitive exclusion between insect pathogenic fungi that occurred from outside to inside the insect hosts. Even being inferior to compete for insects, B. bassiana could outcompete M. robertsii during co-culturing in liquid medium. It was also found that the one-sided mycosis of insects occurred during coinfection with different genotypic strains of either fungi. However, parasexual recombination was evident to take place between the compatible strains after coinfection. The data of this study can help explain the phenomena of the exclusive mycosis of insect individuals, but co-occurrence of entomopathogens in the fields, and suggest that the synergistic effect is questionable regarding the mixed use of fungal parasites for insect pest control.
Phialophora verrucosa (P. verrucosa) is a pathogen that can cause chromoblastomycosis and phaeohyphomycosis. Recent evidence suggests that neutrophils can produce neutrophil extracellular traps (NETs) that can protect against invasive pathogens. As such, we herein explored the in vitro functional importance of P. verrucosa-induced NET formation. By assessing the co-localization of neutrophil elastase and DNA, we were able to confirm the formation of classical NETs entrapping P. verrucosa specimens. Sytox Green was then used to stain these NETs following neutrophil infection with P. verrucosa in order to quantify the formation of these extracellular structures. NET formation was induced upon neutrophil exposure to both live, UV-inactivated, and dead P. verrucosa fungi. The ability of these NETs to kill fungal hyphae and conidia was demonstrated through MTT and pouring plate assays, respectively. Overall, our results confirmed that P. verrucosa was able to trigger the production of NETs, suggesting that these extracellular structures may represent an important innate immune effector mechanism controlling physiological responses to P. verrucosa infection, thereby aiding in pathogen control during the acute phases of infection.
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