[The influence of microtubule intervention drugs on the energy metabolism of myocardial cells after hypoxia].
Nyckelord
Abstrakt
OBJECTIVE
To investigate the influence of microtubule intervention drugs on the energy metabolism of myocardial cells after hypoxia.
METHODS
The primary passage of cultured myocardial cells from neonatal rats were divided into A (with hypoxia), B (with hypoxia and administration of 10 micromol/ml colchicine), C (with hypoxia and administration of 5 micromol/ml taxol), D (with hypoxia and administration of 10 micromol/ml taxol) and E (with hypoxia and administration of 15 micromol/ml taxol) groups. The creatine kinase (CK) activity and contents of ATP and ADP were assayed with colorimetry and HPLC, respectively, and the vitality of myocardial cells were determined by trypan blue method at 0.5, 1.0, 3.0, 6.0, 12.0, 24.0 post-hypoxia hours (PHH).
RESULTS
The mortality was obviously higher in B and E groups than those in A group( P < 0.05) at each time-points, but that in C and D groups were markedly lower than those in A group during 6.0 to 24.0 PHH (P < 0.01). The CK activity was significantly higher in B group than that in A group during 1.0 to 24.0 PHH, while that in E group was evidently higher, but it was lower in C and D groups than that in A group at each time-points (P < 0.05 or 0.01). The ATP contents in C group during 0.5 to 6.0 PHH were [(49.9 +/- 2.8), (40.7 +/- 2.0), (25.8 +/- 1.9), (19.1 +/- 1.2) microg/10(6) cells, respectively], which were obviously higher than those in A group [(42.9 +/- 5.8), (29.5 +/- 1.8), (18.2 +/- 0.9), (14.1 +/- 0.7) microg/10(6) cells, respectively, P < 0.05 or P < 0.01, and those in E group at each time-point were significantly lower than those in A and D groups (P < 0.01). The changes in the contents of ADP were on the contrary to the above.
CONCLUSIONS
Microtubule-destabilizing drugs and high concentration microtubule-stabilizing drugs can sharply decrease ATP content in myocardiocytes under hypoxic conditions, while suitable amount of microtubule-stabilizing drugs can protect myocardiocytes by promoting its energy production.
