Tanshinone IIA sodium sulfonate attenuates inflammation by upregulating circ-Sirt1 and inhibiting the entry of NF-κB into the nucleus

Inflammation is a biological process that exists in a large number of diseases. NF-kappa B has been proven to play a pivotal role in the development of inflammation. New drugs aimed at inhibiting the expression of NF-kappa B have gained attention from researchers. Sirt1 has an anti-inflammatory function, and the circRNA encoded by the Sirt1 gene may also play roles in the anti-inflammatory reaction of Sirt1. In the present study, LPS-treated RAW264.7 cells were used as an inflammatory cell model, and tanshinone IIA sodium sulfonate (TSS) was used as a therapeutic drug. We found that TSS downregulated LPS-induced TNF-alpha and IL-1 beta expression nearly threefold. LPS reduced Circ-sirt1 mRNA expression by one-third, while TSS started this phenomenon. In addition, overexpression/knockdown of Circ-sirt1 neutralized the function of TSS by regulating the translocation of NF-kappa B. Thus, we proved that TSS has an anti-inflammatory function by upregulating circ-Sirt1 and subsequently inhibiting the translocation of NF-kappa B. An in vivo experiment was also performed to confirm the protective function of TSS on inflammation. These results indicated that TSS is a potential treatment for inflammation.

Automated summary

The study found that TSS exerts anti-inflammatory effects by upregulating circ-Sirt1 expression to inhibit the translocation of NF-kappa B. In vivo experiments confirmed the protective function of TSS on inflammation, suggesting that TSS may be a potential treatment for inflammation.