Dynamic expressions of liver tissue apoptosis-related genes of Vibrio vulnificus sepsis rats and the effects of antibacterial agents.
Dynamic changes in mRNA expressions of liver tissue apoptosis-promoting genes Fas and Bax and apoptosis-inhibiting gene Bcl-2 of vibrio vulnificus sepsis rats were detected and the effects of antibacterial agents were examined. The rat model with Vibrio vulnificus sepsis (VV group) was established and some of the Vibrio vulnificus sepsis rats were treated with antibacterial agents (AA group). The mRNA expressions of Fas, Bax and Bcl-2 were measured by reverse transcription polymerase chain reaction (RT-PCR). As compared with normal control group (NC group), the expressions of Fas and Bax mRNA in liver tissue at all different time points in VV group were increased significantly (P<0.05), and the highest levels of Fas and Bax mRNA expressions were 6 and 12 h after the infection, respectively. At the same time, the expression of Bcl-2 mRNA in liver tissue at all different time points in VV group were decreased significantly (P<0.05), and the lowest level of Bcl-2 mRNA expression appeared 2 h after the infection. The mRNA expressions of Bcl-2 in liver tissue 9 and 12 h after the infection in AA group were increased significantly (P<0.05) compared with NC group, while the expressions of Fas and Bax mRNA were not significantly different from those of NC group. Compared with VV group, the expression of Fas mRNA in AA group was decreased (P<0.05) and Bax mRNA was decreased significantly 12 and 16 h after the infection (P<0.05), while the expressions of Bcl-2 mRNA were increased significantly 9, 12 and 16 h after the infection (P<0.05). It is concluded that the mRNA expressions of liver tissue apoptosis-promoting genes Fas and Bax were increased remarkably in vibrio vulnificus sepsis rats, whereas the expression of apoptosis-inhibiting gene Bcl-2 mRNA was decreased obviously in sepsis rats in early stage. The treatment with cefoperazone sodium and levofloxacin lactate could inhibit the expression of Fas mRNA and Bax mRNA and enhance the expression of Bcl-2 mRNA at the same time.
Lu
Zhongqiu
Z
Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. lzq640815@163.com
Li
Mengfang
M
Liang
Huan
H
Qiu
Qiaomeng
Q
Yang
Guangtian
G
Zhou
Tieli
T
Hong
Guangliang
G
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology* / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics*; D005786:Gene Expression Regulation; D008297:Male; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000188:drug therapy* / Q000235:genetics* / Q000382:microbiology; D014735:Vibrio Infections / Q000188:drug therapy / Q000235:genetics; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
D000900:Anti-Bacterial Agents; C494828:Bax protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D019014:fas Receptor