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Basic science: Cardiovascular disease basic research
e0129 Effect of tetrandrine on anoxia/reoxygenation-induced release of proinflammatory factors in cultured cardiocyte of neonate rats
  1. Yuqin Wang,
  2. Yuqin Wang
  1. The Pla 252 hospital


Objective To investigate the effect of tetrandrine on anoxia/reoxygenation-induced the release of myocardial enzyme LDH, CK and proinflammatory factors: TNF-α, IL-1β, IL-6 in cultured cardiocytes of neonate rates.

Methods After cardiocytes were cultured in vitro successfully, it were divided into four group: control group (CON), anoxia/reoxygenation group (A/R), tetrandrine group (Tet), simvastatin (Sim) in random. Each group was treated as follow: CON group - not treated anoxia/reoxygenation, continuous incubated 26 h under normal circumstance. A/R group- first anoxia incubate carried, cells were incubated on the non- saccharide non- serum culture medium, which saturate by 95% argon gases 2 h, reoxygenation incubate followed, cells were incubated in normal circumstance 24 h. 0.9% saline were added into culture fluid before the beginning of reoxygenation. Tet group and Sim group –the procedure of anoxia/reoxygenation was same to A/R group, the difference of these two groups was they added Tet (30 μmol/l) or Sim (10 μmol/l) respectively into culture fluid and incubated 60 min before anoxia beginning. LDH, CK, TNF-α, IL-1β, IL-6 were detected after reoxygenation 24 h.

Result The LDH and CK were increased significantly in A/R, Tet, and Sim groups compared with CON group (p<0.01). The LDH and CK in Tet and Sim group were lower significant than A/R group (p<0.01). 2. The proinflammatory factors TNF-α, IL-1β and IL-6 were increased significantly in A/R, Tet, and Sim groups compared with CON group (p<0.01). And it were lower significant than A/R group (p<0.01). 3. The level of LDH, CK, TNF-α, IL-1β, IL-6 were no significant difference between Tet group and Sim group (p>0.05).

Conclusion Tet can attenuate myocardial ischaemia/reperfusion injury. It achieves this pharmacologic action through inhibition the IκB-α phosphorylation and reduces the harmful cytokine TNF-α and IL-6.

  • Tetrandrine
  • ischaemic/reperfusion injury
  • IκB-α
  • Tumour Necrosis Factor-α
  • Interleukin-6

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