McKinley C J, Turinsky J
Am J Physiol. 1986 Feb;250(2 Pt 2):R207-10. doi: 10.1152/ajpregu.1986.250.2.R207.
Rats were subjected to a single hindlimb scald, and 3 days later soleus muscles from the burned and contralateral unburned hindlimbs were studied in vitro. Burned limb muscle released 354% more prostaglandin E2 (PGE2) and 119% more tyrosine than the contralateral uninjured counterpart. Neither the rate of net proteolysis in the uninjured muscle nor the stimulated net proteolysis in the burned limb muscle could be reduced by 90% inhibition of PGE2 production with aspirin or indomethacin. Inhibition of tissue protein synthesis with 5 X 10(-5) M cycloheximide stimulated tyrosine release by soleus muscles of both hindlimbs, but the increment in the burned limb muscle was 167% greater than in the contralateral uninjured counterpart. Concomitantly, cycloheximide decreased PGE2 releases by injured and uninjured muscles 90 and 73%, respectively. This previously unrecognized action of cycloheximide was investigated in soleus muscles of normal uninjured rats. It was found that 1 X 10(-6) M cycloheximide produces a 70% inhibition of muscle PGE2 release and increasing the concentration of inhibitor up to 500-fold does not further decrease PGE2 production. Cycloheximide acts by reducing the availability of endogenous arachidonic acid for PGE2 synthesis.
将大鼠的单侧后肢进行烫伤，3天后对烫伤侧和对侧未烫伤的后肢比目鱼肌进行体外研究。烫伤侧肢体肌肉释放的前列腺素E2（PGE2）比未受伤的对侧肢体多354%，酪氨酸多119%。用阿司匹林或吲哚美辛抑制PGE2生成90%，既不能降低未受伤肌肉的净蛋白水解速率，也不能降低烫伤侧肢体肌肉受刺激后的净蛋白水解速率。用5×10⁻⁵M放线菌酮抑制组织蛋白合成，刺激了双侧后肢比目鱼肌酪氨酸的释放，但烫伤侧肢体肌肉的增加量比对侧未受伤的肢体大167%。同时，放线菌酮分别使受伤和未受伤肌肉的PGE2释放量减少了90%和73%。在正常未受伤大鼠的比目鱼肌中研究了放线菌酮这种以前未被认识的作用。发现1×10⁻⁶M放线菌酮可使肌肉PGE2释放量减少70%，将抑制剂浓度增加至500倍也不会进一步降低PGE2的生成。放线菌酮通过减少内源性花生四烯酸用于PGE2合成的量来发挥作用。
