Poly(ADP‑ribose) polymerase‑1 inhibitor ameliorates dextran sulfate sodium‑induced colitis in mice by regulating the balance of Th17/Treg cells and inhibiting the NF‑κB signaling pathway
- Shuai Peng
- Lei Shen
- Min-Xiu Tian
- Hui-Min Li
- Shan-Shan Wang
Affiliations: Renmin Hospital of Wuhan University, Hubei Key Laboratory of Digestive System Disease, Wuhan, Hubei 430060, P.R. China
- Published online on: December 10, 2020 https://doi.org/10.3892/etm.2020.9566
Copyright: © Peng
et al. This is an open access article distributed under the
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Poly(ADP‑ribose) polymerase‑1 (PARP‑1) plays a critical role in inflammatory pathways. The PARP‑1 inhibitor, 5‑aminoisoquinolinone (5‑AIQ), has been demonstrated to exert significant pharmacological effects. The present study aimed to further examine the potential mechanisms of 5‑AIQ in a mouse model of dextran sodium sulfate (DSS)‑induced colitis. Colitis conditions were assessed by changes in weight, disease activity index, colon length, histopathology and pro‑inflammatory mediators. The colonic expression of PARP/NF‑κB and STAT3 pathway components was measured by western blot analysis. Flow cytometry was used to analyze the proportion of T helper 17 cells (Th17) and regulatory T cells (Tregs) in the spleen. Western blot analysis and reverse transcription‑quantitative PCR were employed to determine the expression of the transcription factors retinoic acid‑related orphan receptor and forkhead box protein P3. The results demonstrated that 5‑AIQ reduced tissue damage and the inflammatory response in mice with experimental colitis. Moreover, 5‑AIQ increased the proportion of Treg cells and decreased the percentage of Th17 cells in the spleen. Furthermore, following 5‑AIQ treatment, the main components of the PARP/NF‑κB and STAT3 pathways were downregulated. Collectively, these results demonstrate that the PARP‑1 inhibitor, 5‑AIQ, may suppress intestinal inflammation and protect the colonic mucosa by modulating Treg/Th17 immune balance and inhibiting PARP‑1/NF‑κB and STAT3 signaling pathways in mice with experimental colitis.