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.
- ischaemic/reperfusion injury
- Tumour Necrosis Factor-α