[The influence of microtubule intervention drugs on glycolytic key enzymes in myocardial cells after hypoxia].
OBJECTIVE
To investigate the influence of microtubule intervention drugs on glycolytic key enzymes in myocardial cells after hypoxia.


METHODS
The primary passage of cultured myocardial cells from neonatal rats were divided into A group (with hypoxia), B group (with hypoxia and administration of l0 micromol/L colchicine), C group (with hypoxia and administration of 5 micromol/L taxol), D group (with hypoxia and administration of 10 micromol/L taxol), E group (with hypoxia and administration of 15 micromol/L taxol). The morphology of microtubule was observed with laser scanning microscope (LSM). The cell vitality was assayed by cell counting kit (CCK). The activities of hexokinase (HK), pyruvate kinase (PK), phosphofructokinase (PFK) and lactate dehydrogenase (LDH) were assayed with colorimetry.


RESULTS
In group B and E, the microtubule structure was damaged heavily, and the cell vitality was decreased significantly [The cell vitality was (89.99 +/- 3.47)% in B group and (84.56 +/- 6.61)% in E group, respectively, at 1.0 post hypoxia hour (PHH), and hoth values were obviously lower than that in A group (97.44 +/- 1.76)%, P < 0.01]. The HK, PK and PFK activities decreased obviously. The activities of HK, PK and PFK in group C were similar to those of the A group. Compared with that in other groups, the degree of damage of microtubule structure in D group was milden. The activities of HK, PK and PFK in D group during 0.5 - 6.0 PHH were significantly higher than those in A group. The activity of LDH in each group was increased after hypoxia.


CONCLUSIONS
Proper concentration of microtubule-stabilizing drugs can alleviate the damages to microtubule structure, and enhance the activity of glycolytic key enzymes of myocardial cells at early stage of hypoxia.
Teng
Miao
M
Institute of Burn Research, Southwest Hospital, State Key Laboratory of Trauma, Burns and Combined Injury, Third Military Medical University, Chongqing 400038, PR China.
Huang
Yue-Sheng
YS
Dang
Yong-Ming
YM
Fang
Ya-Dong
YD
Zhang
Qiong
Q
D000818:Animals; D015687:Cell Hypoxia; D002478:Cells, Cultured; D006019:Glycolysis / Q000187:drug effects*; D006593:Hexokinase / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008870:Microtubules / Q000187:drug effects* / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000201:enzymology / Q000378:metabolism*; D010732:Phosphofructokinase-1 / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
D007770:L-Lactate Dehydrogenase; D006593:Hexokinase; D010732:Phosphofructokinase-1; D011770:Pyruvate Kinase