[Protective effects of continue insulin infusion on liver mitochondrion in the early stage of septic rats].
OBJECTIVE
To investigate the protective effects of continue insulin infusion on liver mitochondrion and its mechanism in the early stage of lipopolysaccharide-induced septic rats.


METHODS
24 SD rats were randomly divided into 3 groups (An external jugular vein catheterization was performed in every rat a day before intraperitoneal injection): Saline control group (n = 8), LPS group (n = 8) and insulin therapy group (n = 8). Saline control group animals received 9 g/L saline only. LPS group animals were treated with lipopolysaccharide(LPS, 10 mg/kg, i.p.), and then received an infusion of 9 g/L saline at the rate of 1 mL/h. Insulin therapy group animals received an infusion of insulin at the rate of 0.25 U/(kg x h) after being intraperitoneal injected with 10 mg/kg LPS. Blood glucose level was monitored. Blood samples were taken 2 h and 6 h later and the levels of serum TNF-alpha and IL-6 were detected by enzyme-linked immunoadsorbent assay(ELISA). The membrane potential of isolated liver mitochondrion was tested by flow cytometry. The SOD and MDA levels of isolated liver mitochondrion were tested by kit. The morphologic change of mitochondrion in liver was observed by electronic microscopy.


RESULTS
In LPS group, the levels of blood glucose, TNF-alpha, IL-6 and SOD all increased significantly and liver mitochondrial membrane potential decreased significantly compared with control group(P<0.05). In insulin therapy group, the levels of blood glucose, TNF-alpha, IL-6 and SOD all decreased significantly and liver mitochondrial membrane potential increased significantly compared with LPS group(P<0.05). The MDA levels did not differ significantly in the three groups. The mitochondrial ultrastructural changes in every group were not obviously.


CONCLUSIONS
In the early stage of septic rats, reversible liver mitochondrion injury can be observed. Continue insulin infusion can protect liver mitochondrion through attenuating inflammatory reaction and reducing the blood glucose level in septic rats.
Zeng
Qi-yi
QY
Department of Neonate, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zhang
Chun-min
CM
Qian
Xin-hua
XH
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000494:pharmacology; D007262:Infusions, Intravenous; D007274:Injections, Intraperitoneal; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology*; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000633:toxicity; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008854:Microscopy, Electron; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D020011:Protective Agents / Q000008:administration & dosage / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D018805:Sepsis / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D015850:Interleukin-6; D008070:Lipopolysaccharides; D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D013482:Superoxide Dismutase