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Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation.
World J Gastroenterol 2017; 23(7):1180-1188WJ

Abstract

AIM

To investigate the therapeutic effect of Jianpi Qingchang decoction (JPQCD) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice.

METHODS

C57BL/c mice were injected intragastrically with 5% DSS instead of drinking water for 7 d, and their body weight, diarrhea severity and fecal bleeding were monitored, while the mice in the control group were treated with standard drinking water, without DSS. After 7 d, the DSS drinking water was changed to normal water and the DSS group continued with DSS water. The control and DSS groups were given normal saline by intragastric injection. The 5-aminosalicylic acid (5-ASA) group was treated orally with 5-ASA at a dose of 100 mg/kg daily. The JPQCD group was treated orally with JPQCD at a dose of 17.1 g/kg daily. On day 14, the colon length was measured, the colorectal histopathological damage score was assessed, and protein levels of interleukin (IL)-1β, IL-8 and tumor necrosis factor-alpha (TNF-α) in colon supernatants were measured by enzyme-linked immunosorbent assay. mRNA expression of IL-1β, IL-8, TNF-α and nuclear factor-kappa B (NF-κB) was detected by real-time quantitative polymerase chain reaction. Western blotting was used to detect the protein expression of NF-κB and inhibitor of kappa B.

RESULTS

Acute inflammation occurred in the mice administered DSS, including the symptoms of losing body weight, loose feces/watery diarrhea and presence of fecal blood; all these symptoms worsened at 7 d. The colons of mice treated with DSS were assessed by histological examination, and the results confirmed that acute inflammation had occurred, as evidenced by loss of colonic mucosa and chronic inflammatory cell infiltration, and these features extended into the deeper layer of the colon walls. The expression levels of IL-1β, IL-8 and TNF-α in the DSS group were higher than those in the control group (P < 0.05), and the expression levels of IL-1β, IL-8 and TNF-α in the JPQCD and 5-ASA groups were lower than those in the DSS group after treating with JPQCD and 5-ASA. Comparing with the DSS group, the mRNA level of IL-1β, IL-8, TNF-α and NF-κB was significantly reduced by 5-ASA and JPQCD. The difference between JPQCD and 5-ASA groups was not statistically significant (P > 0.05). Comparing with the DSS group, due to using JPQCD and 5-ASA, significant suppression of activation in DSS-induced NF-κB and increased phosphorylation of IκB in mice with experimental colitis occurred (P < 0.05). The difference between the JPQCD group and the 5-ASA group was not statistically significant (P > 0.05).

CONCLUSION

Activation of the NF-κB signaling pathway is inhibited by JPQCD, which shows the potential mechanism by which JPQCD treats UC.

Authors+Show Affiliations

Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.Lie Zheng, Yan-Cheng Dai, Xuan Chen, De-Liang Chen, Yue-Ting Dai, Department of Gastroenterology, Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28275298

Citation

Zheng, Lie, et al. "Jianpi Qingchang Decoction Alleviates Ulcerative Colitis By Inhibiting Nuclear factor-κB Activation." World Journal of Gastroenterology, vol. 23, no. 7, 2017, pp. 1180-1188.
Zheng L, Zhang YL, Dai YC, et al. Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation. World J Gastroenterol. 2017;23(7):1180-1188.
Zheng, L., Zhang, Y. L., Dai, Y. C., Chen, X., Chen, D. L., Dai, Y. T., & Tang, Z. P. (2017). Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation. World Journal of Gastroenterology, 23(7), pp. 1180-1188. doi:10.3748/wjg.v23.i7.1180.
Zheng L, et al. Jianpi Qingchang Decoction Alleviates Ulcerative Colitis By Inhibiting Nuclear factor-κB Activation. World J Gastroenterol. 2017 Feb 21;23(7):1180-1188. PubMed PMID: 28275298.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Jianpi Qingchang decoction alleviates ulcerative colitis by inhibiting nuclear factor-κB activation. AU - Zheng,Lie, AU - Zhang,Ya-Li, AU - Dai,Yan-Cheng, AU - Chen,Xuan, AU - Chen,De-Liang, AU - Dai,Yue-Ting, AU - Tang,Zhi-Peng, PY - 2016/06/30/received PY - 2016/09/13/revised PY - 2016/10/10/accepted PY - 2017/3/10/entrez PY - 2017/3/10/pubmed PY - 2017/8/15/medline KW - Dextran sodium sulfate KW - Inflammation KW - Jianpi Qingchang decoction KW - Nuclear factor-κB KW - Ulcerative colitis SP - 1180 EP - 1188 JF - World journal of gastroenterology JO - World J. Gastroenterol. VL - 23 IS - 7 N2 - AIM: To investigate the therapeutic effect of Jianpi Qingchang decoction (JPQCD) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. METHODS: C57BL/c mice were injected intragastrically with 5% DSS instead of drinking water for 7 d, and their body weight, diarrhea severity and fecal bleeding were monitored, while the mice in the control group were treated with standard drinking water, without DSS. After 7 d, the DSS drinking water was changed to normal water and the DSS group continued with DSS water. The control and DSS groups were given normal saline by intragastric injection. The 5-aminosalicylic acid (5-ASA) group was treated orally with 5-ASA at a dose of 100 mg/kg daily. The JPQCD group was treated orally with JPQCD at a dose of 17.1 g/kg daily. On day 14, the colon length was measured, the colorectal histopathological damage score was assessed, and protein levels of interleukin (IL)-1β, IL-8 and tumor necrosis factor-alpha (TNF-α) in colon supernatants were measured by enzyme-linked immunosorbent assay. mRNA expression of IL-1β, IL-8, TNF-α and nuclear factor-kappa B (NF-κB) was detected by real-time quantitative polymerase chain reaction. Western blotting was used to detect the protein expression of NF-κB and inhibitor of kappa B. RESULTS: Acute inflammation occurred in the mice administered DSS, including the symptoms of losing body weight, loose feces/watery diarrhea and presence of fecal blood; all these symptoms worsened at 7 d. The colons of mice treated with DSS were assessed by histological examination, and the results confirmed that acute inflammation had occurred, as evidenced by loss of colonic mucosa and chronic inflammatory cell infiltration, and these features extended into the deeper layer of the colon walls. The expression levels of IL-1β, IL-8 and TNF-α in the DSS group were higher than those in the control group (P < 0.05), and the expression levels of IL-1β, IL-8 and TNF-α in the JPQCD and 5-ASA groups were lower than those in the DSS group after treating with JPQCD and 5-ASA. Comparing with the DSS group, the mRNA level of IL-1β, IL-8, TNF-α and NF-κB was significantly reduced by 5-ASA and JPQCD. The difference between JPQCD and 5-ASA groups was not statistically significant (P > 0.05). Comparing with the DSS group, due to using JPQCD and 5-ASA, significant suppression of activation in DSS-induced NF-κB and increased phosphorylation of IκB in mice with experimental colitis occurred (P < 0.05). The difference between the JPQCD group and the 5-ASA group was not statistically significant (P > 0.05). CONCLUSION: Activation of the NF-κB signaling pathway is inhibited by JPQCD, which shows the potential mechanism by which JPQCD treats UC. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/28275298/Jianpi_Qingchang_decoction_alleviates_ulcerative_colitis_by_inhibiting_nuclear_factor_κB_activation_ L2 - http://www.wjgnet.com/1007-9327/full/v23/i7/1180.htm DB - PRIME DP - Unbound Medicine ER -