Effects of Manbai Shengfa formula on intestinal flora in mice with androgenic alopecia

Objective To investigate the effects of Manbai Shengfa formula on intestinal flora in mice with androgenic alopecia (AGA), using 16S rDNA technology. Methods A total of 36 C57BL/6 mice were randomly divided into 6 groups, i.e. blank control group, model group, positive control group, and high-, medium-, and low-dose of Manbai Shengfa formula, with 6 mice per group. Following removal of hair on the back (2 cm × 3 cm area), multiple-point subcutaneous injections of testosterone propionate at a total dose of 0.1 mg/d/mouse were given to establish the AGA model, while the uninjected mice served as blank controls. Afterward, both the blank controls and model mice were treated topically with normal saline (1.0 mL/d/ mouse). The positive group was treated topically with 5% minoxidil tincture (1.0 mL/d/ mouse). The rest three groups were treated orally with Manbai Shengfa formula at doses of 5.0 g/kg, 2.5 g/kg and 1.25 g/kg, respectively, for 30 consecutive days. After 30-day treatments, the skin of the depilated area was collected for pathology, and the feces were collected for 16S rDNA analysis. Results Compared with the untreated model group, Manbai Shengfa formula significantly increased the number of hair follicles. The morphology of hair follicles in the high-dose group was similar to that in the blank controls. The results of diversity analysis showed that the model group exhibited a reduced richness and diversity of intestinal flora compared to the blank controls, while Manbai Shengfa formula dose-dependently increased the richness of intestinal flora in the mouse model of AGA. The alpha diversity indices of intestinal flora differed significantly between the model group and the Manbai Shengfa formula treated groups (P<0.05). Conclusions Manbai Shengfa formula can significantly increase the richness and diversity of intestinal flora. The therapeutic effects of Manbai Shengfa formula for alopecia in AGA model may be linked to the regulation of intestinal microbial diversity.