Acne is a common problem in dermatologic clinics. The pathogenesis of acne involves various factors, such as increased sebum production and alteration of the quality of sebum lipids caused by increased androgen activity, abnormal keratinization of the infundibular epithelium, colonization of Propionibacterium acnes (P. acnes) within the follicles, and the inflammation process. 1 P. acnes may stimulate sebaceous glands via the toll-like receptors (TLRs), mainly TLR2.Keratinocytes and monocytes in acne lesions also express TLR2 on the surface. The TLR2-dependent pathway activation leads to a triggering of the nuclear transcription factor and then produces multiple cytokines and chemokines such as IL-1, IL-8, IL-12, and TNFα. 2 Furthermore, P. acnes can release various exogenous proteases by activating the protease-activated receptor-2 or PAR-2 on the keratinocyte surface. These proteases can enhance the transcription of pro-inflammatory cytokines, for instance IL-1a, IL-8, TNFα, and a variety of matrix metalloproteinases. 1 Currently, numerous treatment options are available, but acne remains a chronic inflammatory disease. Concerning adverse effects of conventional medicines, alternative medications with antiinflammatory effects have increased in popularity. 3