[Effect of N-acetylcysteine on lipopolysaccharide induced preterm labor in mice].
OBJECTIVE
To test the effect of N-acetylcysteine (NAC) on the mice with infection associated preterm labor.


METHODS
The pregnant C57BL/6 mice were randomly distributed into five groups, each with 20 mice and were given lipopolysaccharide (LPS), saline solution (NS), NAC, LPS+NAC (therapy), and NAC+ LPS (prevention) respectively. The LPS (20 microg) was injected intraperitoneally to the mice every 12 hours since day 16 of gestation to induce preterm labor. The NAC was orally administered (0.5 g/kg) every 12 hours since day 15 or day 16 for the prevention and therapy groups respectively. The latency interval (from LPS injection to delivery of the first pup) and fetal survival rates were recorded in eight mice from each group. The remaining mice were killed at 4, 8, 12, and 24 hours after the LPS injection (three for a group each time). The NF-kappaB activity and IL-8 mRNA in uterine and maternal and fetal hepatic GSH-PX and serum IL-8, MDA, and SOD were examined.


RESULTS
The average latency interval of LPS-treated mice was (15.1 +/- 1.9) hours, with a fetal survival rate of 4.3%. The NAC therapy extended the latency interval of LPS-treated mice to (35.4 +/- 2.1) hours, with a fetal survival rate of 69.0%. The NAC prevention extended the latency interval of LPS-treated mice to (44.8 +/- 2.6) hours, with a fetal survival rate of 84.3%. The expression of NF-KB P65 was activated and reached the peak 4 hours after the LPS injection. The uterine IL-8 mRNA and serum IL-8 and MDA reached the peak whereas the maternal and fetal hepatic GSH and SOD declined to the lowest 8 hours after the LPS injection. The NAC significantly inhibited the effect induced by the LPS (P < 0.01).


CONCLUSIONS
The NAC has a therapeutic effect on the LPS-induced preterm labor in mice. It is even better to be used in preventing preterm labor. The mechanism of the protective effect of NAC may include the deactivation of the NF-kappaB/IL-8 and the reduce of the production of ROS.
Jiang
Xue-Feng
XF
Department of Obstetrics and Gynecology, The first Affiliated Hospital, Jinan University, Guangzhou 510630, China.
Zeng
Wei-Yue
WY
Yang
Kai-Xuan
KX
Xu
Zhi-Hong
ZH
Xu
Ai-Qun
AQ
D000111:Acetylcysteine / Q000494:pharmacology* / Q000627:therapeutic use / Q000633:toxicity; D000818:Animals; D005260:Female; D005333:Fetus / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D007239:Infections / Q000150:complications; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D007752:Obstetric Labor, Premature / Q000139:chemically induced* / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D010084:Oxidation-Reduction / Q000187:drug effects; D011247:Pregnancy; D012333:RNA, Messenger; D051996:Transcription Factor RelA / Q000378:metabolism
D016209:Interleukin-8; D008070:Lipopolysaccharides; D012333:RNA, Messenger; C498144:Rela protein, mouse; D051996:Transcription Factor RelA; D000111:Acetylcysteine