[Effect of oxymatrine on JAK2/STAT3 signaling in renal tissues of rats with septic shock]

Zhongguo Zhong Yao Za Zhi. 2013 Aug;38(16):2696-700.
[Article in Chinese]

Abstract

Objective: To explore the effect of oxymatrine (OMT) on JAK2/STAT3 signaling in renal tissues of rats with septic shock.

Method: The cecal ligation and puncture (CLP) was adopted to establish the rat septic shock model. Fifty-six male SD rats were randomly divided into 7 groups: the sham operation group, the model (CLP) group, CLP + OMT high, middle, low-dose (52, 26, 13 mg x kg(-1), vena caudalis bolus) groups and the positive control (CLP + dexamethasone, 10 mg x kg(-1)) group. The pathological changes in renal tissues were examined with lightmicroscope. BUN content was determined by urine enzymatic method. Expressions of tumournecrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA in renal tissues were determined by RT-PCR. Expression of JAK2 and STAT3 in renal tissues determined by Western blot. Changes in tumournecrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) contents in renal tissue were determined by radioimmunoassay.

Result: OMT of different doses could inhibit the JAK2 and STAT3 activation in renal tissues (P<0.05), and decrease the protein expression of JAK2, STAT3, TNF-alpha and IL-1beta mRNA (P<0.05). Besides, it could reduce TNF-alpha and IL-1beta contents in renal tissue homogenate (P<0.05), serum BUN content (P<0.05), and improve such lesions as tissue hyperemia, edema and inflammatory cell infiltration, with identical results in medium and high-dose OMT groups, and the positive control group.

Conclusion: OMT can inhibit JAK2/STAT3 signaling activity to reduce the expression of proin-flammatory factors (TNF-alpha, IL-1beta) and treat the renal injury in rats with septic shock.

MeSH terms

  • Alkaloids / pharmacology*
  • Animals
  • Gene Expression Regulation / drug effects
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Janus Kinase 2 / metabolism*
  • Kidney / drug effects*
  • Kidney / metabolism
  • Kidney / pathology*
  • Male
  • Quinolizines / pharmacology*
  • Rats
  • Rats, Sprague-Dawley
  • STAT3 Transcription Factor / metabolism*
  • Shock, Septic / blood
  • Shock, Septic / metabolism
  • Shock, Septic / pathology*
  • Signal Transduction / drug effects*
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Alkaloids
  • Interleukin-1beta
  • Quinolizines
  • STAT3 Transcription Factor
  • Tumor Necrosis Factor-alpha
  • oxymatrine
  • Janus Kinase 2