Curcumin regulated shift from Th1 to Th2 in trinitrobenzene sulphonic acid-induced chronic colitis

Acta Pharmacol Sin. 2006 Aug;27(8):1071-7. doi: 10.1111/j.1745-7254.2006.00322.x.


Aim: To investigate the therapeutic effects of curcumin (Cur) on trinitrobenzene sulphonic acid (TNBS)-induced colitis and the effects of Cur on the balance of Th1/Th2 cytokines.

Methods: Colitis was induced by TNBS and treated with Cur (30 mg/kg/d, ip), dexamethasone (Dex, 2 mg/kg/d), or Cur plus dexamethasone (Cur+Dex, 30 mg/kg/d Cur ip+2 mg/kg/d Dex,ip). mRNA in colon mucosa were detected by real-time quantitative polymerase chain reaction. Intracellular cytokines were detected by flow cytometry and concentrations of cytokines in sera were detected by enzyme-linked immunosorbent analysis.

Results: Both Cur and Dex improved body weight loss, ameliorated histological images and decreased macroscopic score and myeloperoxidase activity. Cur decreased the expression of Th1 cytokines (IL-12, IFN-gamma, TNF-alpha, IL-1) and increased the expression of Th2 cytokines (IL-4 and IL-10) in colon mucosa. Cur also increased the proportion of IFN-gamma/IL-4 in splenocytes and circulation. Dex and Cur+Dex decreased the expression of Th1 cytokines but could not increase the expression of Th2 cytokines and the proportion of IFN-gamma/IL-4.

Conclusion: Cur exerted therapeutic effects on colitis by regulating the shift from Th1 to Th2.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Colitis / chemically induced
  • Colitis / metabolism*
  • Colitis / pathology
  • Colon / metabolism
  • Colon / pathology
  • Curcumin / pharmacology*
  • Cytokines / biosynthesis*
  • Cytokines / genetics
  • Dexamethasone / pharmacology
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / genetics
  • Interleukin-12 / biosynthesis
  • Interleukin-12 / genetics
  • Intestinal Mucosa / metabolism*
  • Peroxidase / metabolism
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Rats
  • Rats, Sprague-Dawley
  • Trinitrobenzenesulfonic Acid
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / genetics


  • Anti-Inflammatory Agents
  • Anti-Inflammatory Agents, Non-Steroidal
  • Cytokines
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interleukin-12
  • Dexamethasone
  • Interferon-gamma
  • Trinitrobenzenesulfonic Acid
  • Peroxidase
  • Curcumin