[Study on mechanisms of mitochondria in lymphocyte apoptosis of sepsis].
OBJECTIVE
To investigate cell apoptosis, mitochondrial membrane potential, cytochrome C and mechanisms of mitochondria in lymphocyte apoptosis of sepsis.


METHODS
In the research, female C57BL/6 mice whose body weight ranged from 17 to 25 grams were utilized and assigned randomly to two groups: sham operated group (Control), cecal ligation and puncture group (CLP). The present study was undertaken by using the mice splenic lymphocyte to investigate cell apoptosis, mitochondrial membrane potential, cytochrome C. The apoptosis alteration was evaluated by Annexin V-FITC/PI double staining with flow cytometry. The alteration of mitochondrial membrane potential was investigated by Rhodamine-123 staining of cells. Cytochrome C of mitochondria and cytosol was investigated by Western blot methods. Statistical analysis was performed using SPSS 11.5 for Windows software. Experiment data was indicated with mean ± standard.


RESULTS
The splenic lymphocyte apoptosis was significantly accelerated in the CLP group when compared with that in control group (17.3% ± 2.2% vs. 3.5% ± 0.5%, P < 0.05). The Rhodamine-123 fluorescent intensity in splenic lymphocyte apoptosis was reduced in CLP group (76.2% ± 1.6%). Comparison between sham group (99.6% ± 0.4%) and CLP group had statistical significance (P < 0.05). Apoptosis could induce mitochondrial cytochrome C release into cytoplasm. In the CLP group, elevation of cytochrome C in cytosol was concurrently in accordance with decline in mitochondrial cytochrome C content.


CONCLUSIONS
These data suggest that mitochondria and mitochondria signal pathway play an important role in lymphocyte apoptosis of sepsis.
Department of General Surgery, Tianjin Haihe Hospital, Tianjin, China.
Li
L
Li
Tao
T
Ma
Wen-quan
WQ
Hu
Lu
L
Han
Zhong
Z
Wang
D000818:Animals; D017209:Apoptosis; D002478:Cells, Cultured; D045304:Cytochromes c / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D008214:Lymphocytes / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000378:metabolism / Q000502:physiology*; D018805:Sepsis / Q000378:metabolism / Q000473:pathology*
D045304:Cytochromes c