Tanshinol relieves lipopolysaccharide‐induced inflammatory injury of HaCaT cells via down‐regulation of microRNA‐122

This study investigated the effects of tanshinol (TAN) on lipopolysaccharide (LPS)‐induced human keratinocytes inflammatory injury and underlying potential molecular mechanisms. Viability and apoptosis of HaCaT cells were assessed using MTT assay and Annexin V‐FITC/PI staining, respectively. Quantitative reverse transcription–polymerase chain reaction was performed to measure the expression of microRNA‐122 (miR‐122) in HaCaT cells. Cell transfection was conducted to up‐regulate the expression of miR‐122. Western blotting was used to detect the protein expression levels of key factors involved in cell apoptosis, inflammatory response, c‐Jun N‐terminal kinase (JNK), and nuclear factor kappa B (NF‐κB) pathways. We found that LPS treatment induced HaCaT cell inflammatory injury by inhibiting cell viability, promoting cell apoptosis, and enhancing the protein expression levels of cyclooxygenase 2 and inducible nitric oxide synthase. TAN treatment relieved LPS‐induced HaCaT cell inflammatory injury. Moreover, TAN treatment attenuated LPS‐induced activation of JNK and NF‐κB pathways in HaCaT cells. Furthermore, TAN treatment alleviated LPS‐induced up‐regulation of miR‐122. Overexpression of miR‐122 reversed the effects of TAN on LPS‐induced HaCaT cell inflammatory injury and activation of JNK and NF‐κB pathways. In conclusion, TAN exerted anti‐inflammatory and protective effects on keratinocytes injury. TAN relieved LPS‐induced inflammatory injury of human HaCaT cells via down‐regulating miR‐122 and then inactivating JNK and NF‐κB pathways.