ObjectiveTo investigate the effects of Sanjie Quban prescription （SJQB）-containing serum on the proliferation， apoptosis， migration， and invasion of human keloid fibroblasts （KFs） and to elucidate its underlying mechanism， with a focus on the aryl hydrocarbon receptor （AhR）/cytochrome P450 family 1 subfamily A member 1 （CYP1A1） signaling pathway. MethodsPrimary human KFs were cultured in vitro and assigned to the following groups： control （KFs+blank serum）， asiaticoside （KFs+asiaticoside-containing serum）， SJQB （KFs+SJQB-containing serum）， AhR agonist （KFs+β-naphthoflavone）， AhR inhibitor （KFs+CH223191）， and AhR inhibitor+SJQB （KFs+CH223191+SJQB-containing serum）. The optimal intervention concentrations were determined through the cell counting kit-8 （CCK-8） assay. Cell proliferation， apoptosis， migration， and invasion were evaluated by the EdU assay， flow cytometry， wound healing assay， and Transwell assay， respectively. The expression of transforming growth factor-β₁ （TGF-β₁） and α-smooth muscle actin （α-SMA） was visualized by immunofluorescence. The mRNA and protein levels of AhR， CYP1A1， TGF-β₁， and α-SMA were measured by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. ResultsCompared with the control group， the SJQB， asiaticoside， and AhR agonist groups demonstrated inhibited cell proliferation， migration， and invasion， along with an increased apoptosis rate （P<0.01）. The AhR inhibitor group showed enhanced proliferation， migration， and invasion together with a reduced apoptosis rate in comparison with the AhR agonist group （P<0.01）. The AhR inhibitor+SJQB group exhibited increased proliferation， migration， and invasion as well as decreased apoptosis compared with the SJQB group （P<0.05， P<0.01）. At the molecular level， compared with the control group， the SJQB， asiaticoside， and AhR agonist groups presented upregulated protein and mRNA levels of AhR and CYP1A1 （P<0.05， P<0.01）， while the SJQB and AhR agonist groups showed downregulated TGF-β₁ and α-SMA expression at both protein and mRNA levels （P<0.05， P<0.01）， and the asiaticoside group displayed decreased protein level of TGF-β₁ and mRNA level of α-SMA （P<0.05， P<0.01）. Compared with both the AhR agonist and control groups， the AhR inhibitor group exhibited decreased AhR and CYP1A1 expression but increased TGF-β₁ and α-SMA expression at protein and mRNA levels （P<0.01）. In comparison with the SJQB group， the AhR inhibitor+SJQB group demonstrated reduced AhR and CYP1A1 expression （P<0.01） and elevated TGF-β₁ and α-SMA expression （P<0.05， P<0.01） at both protein and mRNA levels. ConclusionSJQB may activate the AhR/CYP1A1 signaling pathway to downregulate TGF-β₁ and α-SMA expression， thereby suppressing the proliferation， migration， and invasion and inducing the apoptosis of KFs.

Based on the discussion of "eight weak areas" in The Inner Canon of Yellow Emperor （《黄帝内经》）， combined with the typical rash manifestations of atopic dermatitis， it is believed that atopic dermatitis is mostly deficiency-excess complex， and that pathogens intruding eight weak areas are the core of its pathogenesis. The external cause is exterior deficiencies， with heat， wind， dampness and other pathogenic qi attacking. The heart， lungs， kidneys out of balance， and excess pathogen are the internal cause， in which fire constraint and excessive heat are the basis of the disease， the wind invading leads to the progress of the changes， dampness obstructing channels and colla-terals make the condition persistent. Internal and external pathogens combination and retention result to the course of the disease lingering and difficult to cure. The internal treatment is to regulate zang-fu organs， and the formula could use self-prescribed modified Qingrun Tongluo Decoction （清润通络汤）， clearing heart and reducing fire in order to clear the heat and cool the blood， moistening lungs and generating metal to consolidate the exterior and dispel the wind， and nourishing kidneys and draining water to dispel the dampness and activate the collaterals. The external treatment applies maceration， fire acupuncture， wrapping to dredge the eight weak areas and regulate qi and blood in channel， so as to expel pathogens.

Objective To evaluate the efficacy of Qingfei-Jiedu decoction in the treatment of Acne. Methods A total of 93 female patients with acne were randomly divided into 3 groups according to random number table, 31 in each group. The observation group took the oral Qingfei-Jiedu decoction, and the Chinese medicine control group took the oral tanshinone capsule, and the western medicine control group took the oral acetic acid ring propyl alcohol progesterone. All 3 groups were treated for 4 weeks. The levels of serum dihydro (DHT), IL-6 and IL-8 were measured by ELISA. The changes of the lesions before and after treatment were observed and the adverse events were recorded during the treatment. The clinical effect was evaluated. Results After treatment, the serum DHT (56.94 ± 15.74 pg/ml vs. 74.48 ± 18.53 pg/ml, t=2.089), IL-6 (22.84 ± 11.77 pg/ml vs. 30.37 ± 14.50 pg/ml, t=2.135), IL-8 (22.64 ± 7.38 pg/ml vs. 29.54 ± 9.65 pg/ml, t=2.057) in the observation group were significantly lower than those in the Chinese medicine control group (P<0.05). After treatment, the disappearance rate of skin lesions (65.4% ± 15.0% vs. 44.7% ± 12.9%, 42.7% ± 13.6%, F=6.862) and comprehensive syndrome effective rate (57.2% ± 12.6% vs. 46.3% ± 12.8%, 44.8% ± 11.7%, F=5.322) in the observation group were significantly higher than those in the other two control groups (P<0.05). The observation group and the traditional Chinese medicine control group did not have adverse events, but the western medicine control group showed one case nausea. Conclusions The Qingfei-Jiedu decoction can reduce the level of serum DHT, IL-6 and IL-8 in female patients with acne vulgaris, and improve the skin lesion disappearance rates and comprehensive syndrome rates.