Login / Signup

Surfactin-oleogel with therapeutic potential for inflammatory acne vulgaris induced by Propionibacterium acnes.

Mengyuan ShanFanqiang MengChao TangLibang ZhouZhaoxin LuYingjian Lu
Published in: Applied microbiology and biotechnology (2021)
Accumulating evidence suggested that suppression of Propionibacterium acnes-induced inflammation was a promising strategy to alleviate acne vulgaris. This study evaluated the alleviating effect of surfactin-oleogel on P. acnes-induced inflammatory acne vulgaris in mice. Epidermis morphology and histopathological examination showed that surfactin-oleogel effectively ameliorated the P. acnes-induced epidermis swelling and erythema. Surfactin-oleogel reduced the epidermis thickness to 48.52% compared to the model control group. The colony of P. acnes in the epidermis was decreased by 1 log CFU/mL after receiving surfactin-oleogel treatment. Furthermore, surfactin-oleogel attenuated oxidative stress in the epidermis by increasing the activities of superoxide dismutase, catalase, and glutathione peroxidase. In addition, the expression of inducible nitric oxide synthase, nitric oxide, cyclooxygenase-2, pro-inflammatory cytokines (e.g. tumour necrosis factor-α and interleukin-1β), and nuclear factor kappa-B in the epidermis were reduced after treating with surfactin-oleogel. Moreover, total cholesterol and free fatty acids were decreased, whereas the treatment of surfactin-oleogel increased triglycerides and linoleic acid content. Besides, immunohistochemical assay and real-time PCR analysis indicated that surfactin-oleogel blocked the TLR2-mediated NF-κB signalling pathways in the epidermis. Consequently, our results demonstrated that surfactin-oleogel had antibacterial and anti-inflammation activities to treat P. acnes-induced inflammatory acne vulgaris.Key points• Surfactin-oleogel effectively relieves inflammation and oxidative stress caused by P. acnes.• Surfactin-oleogel effectively reduced the P. acnes colony.• Surfactin-oleogel relieves P. acnes-induced inflammation by inactivated the TLR-mediated NF-κB.
Keyphrases