Cutaneous and ocular toxicology · 2026
Yangxuebushen Decoction prevents cyclophosphamide-induced hair loss by inhibiting hair follicle apoptosis.
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Sun Yunyun, Wei Yuegang, Ren Hui, Shi Xiaochen
Аннотация
BACKGROUND: Alopecia is a skin condition that can impose a substantial psychological burden on affected individuals, and chemotherapy-induced alopecia remains one of the most distressing adverse effects of anticancer treatment. Since antiquity, medicinal plants have been widely used in traditional Chinese medicine to support hair growth. In the present study, we investigated whether Yangxuebushen Decoction (YXBSD) could promote hair regrowth and mitigate alopecia in a cyclophosphamide (CYP)-induced mouse model.
METHODS: A CYP-induced alopecia model was established in C57BL/6J mice (n = 5). Mice were allocated to a control group, a CYP group, and a CYP + YXBSD intervention group. The effects of YXBSD on hair growth and related biological processes were assessed through macroscopic observation and histopathologic evaluation, as well as TUNEL staining, immunofluorescence, immunohistochemistry, and real-time fluorescence quantitative PCR to examine hair follicle structure, apoptosis, inflammation, and oxidative stress.
RESULTS: YXBSD significantly promoted hair growth in CYP-treated mice, improved hair follicle architecture, increased the proportion of hair follicles in the growth phase (from 15% to 30%), and reduced apoptosis of hair follicle cells (from 30% to 20%). In parallel, YXBSD markedly suppressed the expression of inflammatory mediators (TNF-α, IL-6, and IL-1β) in skin tissue, decreased the oxidative stress marker malondialdehyde (MDA), and increased the activity of the antioxidant enzyme superoxide dismutase (SOD). Consistent with these changes, YXBSD upregulated the proliferation marker Ki-67 while downregulating the apoptosis-related protein p53.
CONCLUSION: YXBSD effectively alleviated CYP-induced alopecia by inhibiting apoptosis in hair follicle cells while concurrently reducing inflammation and oxidative stress, thereby promoting the recovery of hair follicle structure and function. These findings suggest that YXBSD has potential as an adjuvant intervention for chemotherapy-induced alopecia.
METHODS: A CYP-induced alopecia model was established in C57BL/6J mice (n = 5). Mice were allocated to a control group, a CYP group, and a CYP + YXBSD intervention group. The effects of YXBSD on hair growth and related biological processes were assessed through macroscopic observation and histopathologic evaluation, as well as TUNEL staining, immunofluorescence, immunohistochemistry, and real-time fluorescence quantitative PCR to examine hair follicle structure, apoptosis, inflammation, and oxidative stress.
RESULTS: YXBSD significantly promoted hair growth in CYP-treated mice, improved hair follicle architecture, increased the proportion of hair follicles in the growth phase (from 15% to 30%), and reduced apoptosis of hair follicle cells (from 30% to 20%). In parallel, YXBSD markedly suppressed the expression of inflammatory mediators (TNF-α, IL-6, and IL-1β) in skin tissue, decreased the oxidative stress marker malondialdehyde (MDA), and increased the activity of the antioxidant enzyme superoxide dismutase (SOD). Consistent with these changes, YXBSD upregulated the proliferation marker Ki-67 while downregulating the apoptosis-related protein p53.
CONCLUSION: YXBSD effectively alleviated CYP-induced alopecia by inhibiting apoptosis in hair follicle cells while concurrently reducing inflammation and oxidative stress, thereby promoting the recovery of hair follicle structure and function. These findings suggest that YXBSD has potential as an adjuvant intervention for chemotherapy-induced alopecia.