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.
Keywords: JNK pathway; NF-κB pathways; lipopolysaccharide; microRNA-122; pressure ulcers; tanshinol.
© 2019 John Wiley & Sons, Ltd.