Objective To research the protective effect of insulin(IN)on lipopolysaccharide(LPS)- induced impairments of rat cardiomyocytes H9c2,and the role of uncoupling protein 2(UCP2)in this process. Methods Using randomized controlled grouping,after cultured for 24 h,H9c2 cells were randomly divided into 5 groups as follows:con-trol group,LPS stimulation group(LPS group),LPS + 70 IU/ L IN group(IN 70 IU/ L group),LPS + 350 IU/ L IN group(IN 350 IU/ L group),and LPS + 700 IU/ L IN group(IN 700 IU/ L group). H9c2 cells in IN group were treated with 70 IU/ L,350 IU/ L or 700 IU/ L IN 15 min before LPS stimulation,and H9c2 cells in control group were treated with an equal volume of saline. After that,cells in group LPS and IN were treated with LPS for 24 h. Lactate dehydro-genase(LDH)in the culture was determined with LDH detecting assay kit. The activity of reactive oxygen species (ROS)and superoxide dismutase(SOD),and content of malonaldehyde(MDA)were determined by colorimetric detec-tion. Cell viability was evaluated by cell count kit - 8. The expressions of UCP2 in transcription and translation levels were detected through transcription polymerase chain reaction and Western blot respectively. Results The levels of LDH,MDA,and intracellular ROS in LPS group significantly increased compared with control group[LDH:(829. 3 ± 75. 3)U/ L vs(223. 5 ± 23. 6)U/ L,MDA:(60. 90 ± 5. 73)nmol/ mgprot vs(19. 70 ± 1. 99)nmol/ mgprot,ROS:(410. 2 ± 81. 6)U/ well vs(94. 3 ± 18. 5)U/ well,all P ﹤ 0. 05)],while the cell viability and SOD activity significantly decreased[cell viability:0. 822 ± 0. 058 vs 1. 012 ± 0. 023,SOD:(49. 20 ± 5. 81)U/ mgprot vs(89. 80 ± 2. 57)U/ mg-prot,all P ﹤ 0. 05]. And the mRNA and protein expressions of UCP2 in LPS stimulation group were up - regulated (1. 867 ± 0. 130 vs 1. 028 ± 0. 097,0. 288 ± 0. 018 vs 0. 180 ± 0. 008,all P ﹤ 0. 05). 350 IU/ L and 700 IU/ L IN inter-vention significantly decreased the levels of LDH,MDA and intracellular ROS[LDH:(568. 2 ± 35. 7)U/ L,(622. 8 ± 27. 6)U/ L vs(829. 3 ± 75. 3)U/ L,MDA:(29. 20 ± 4. 20)nmol/ mgprot,(42. 10 ± 2. 32)nmol/ mgprot vs(60. 90 ± 5. 73)nmol/ mgprot,ROS:(270. 3 ± 46. 8)U/ well,(301. 5 ± 16. 9)U/ well vs(410. 2 ± 81. 6)U/ well,all P ﹤ 0. 05], increased the cell survival and the levels of SOD activity[cell viability:0. 960 ± 0. 029,0. 906 ± 0. 039 vs 0. 822 ± 0. 058,SOD:(75. 20 ± 2. 21)U/ mgprot,(61. 20 ± 3. 38)U/ mgprot vs(49. 20 ± 5. 81)U/ mgprot,all P ﹤ 0. 05]. And IN with 350 IU/ L and 700 IU/ L increased the mRNA and protein expression of UCP2(3. 830 ± 0. 265,2. 855 ± 0. 215 vs 1. 867 ± 0. 130,0. 464 ± 0. 215,0. 355 ± 0. 006 vs 0. 288 ± 0. 018,all P ﹤ 0. 05). Compared with 70 IU/ L and 700 IU/ L IN group,350 IU/ L IN group had better results. Conclusions IN attenuates LPS - induced oxidative injury in H9c2 cells,which is probably mediated through up - regulating the expression of UCP2.

ObjectiveTo investigate the effects of autophagy on exocrine function of pancreas in rats with acute sepsis, and to determine whether the mitochondrial coenzyme Q (Mito Q) can prevent exocrine dysfunction of pancreas mediated by autophagy.Methods ExperimentⅠ: 30 Sprague-Dawley (SD) rats were randomly divided into three groups, with 10 rats in each group. All the rats were given lipopolysaccharide (LPS, 10 mg/kg) intraperitoneally, and Wortmannin (2 mg/kg), the specific inhibitor of autophagy (LPS+ Wortmannin group), Mito Q (6.5μmol/kg, LPS+Mito Q group), or the same volume of normal saline (LPS group) was respectively injected via the tail vein 1 hour later. Survival rate was assessed within 12 hours after LPS injection. ExperimentⅡ: another 100 male SD rats were randomly divided into ten groups with 10 rats in each group: namely control 4, 6 and 12 hours groups, LPS 4, 6 and 12 hours groups, and LPS+ Wortmannin 4 hours group, Wortmannin 4 hours group, LPS+ Mito Q 6 hours group, and Mito Q 6 hours group. The protocols of model reproduction and drug administration were the same as in the experimentⅠ. Blood samples were collected at each time point, and the amylase content was determined with the velocity method. The levels of reactive oxygen species (ROS) in the pancreases were measured with enzyme-linked immunosorbent assay (ELISA). The expression of the autophagy-related protein LC3 was determined with Western Blot. The pathological changes in the pancreas were observed with microscopy.Results① The survival time in the LPS+ Wortmannin group was significantly shorter than that in the LPS group (hours: 7.50±0.64 vs. 11.90±0.13,χ2= 19.847,P= 0.001). There was no significant difference in the survival time between LPS+ Mito Q and LPS groups (hours: 11.60±0.24 vs. 11.90±0.13,χ2= 1.055,P= 0.137).② The serum amylase in the LPS 6 hours, LPS+ Wortmannin 4 hours, and LPS+ Mito Q 6 hours groups were significantly higher than those in the control group at the same time points (U/L:2 881.00±550.12 vs. 2 099.20±249.57, 3 672.00±779.24 vs. 2 081.36±245.18, 2 975.20±687.03 vs. 2 099.20± 249.57, allP< 0.05), and were significantly lowered in LPS 12 hours group (U/L: 794.00±218.71 vs. 2 086.80±261.75, P< 0.01). The pancreatic ROS in the LPS 6 hours and 12 hours groups, LPS+ Wortmannin 4 hours group, and LPS+Mito Q 6 hours group were significantly higher than those of the control group at the same time points (kU/L: 3.18±1.06 vs. 1.78±0.37, 3.63±1.08 vs. 1.85±0.41, 3.14±0.98 vs. 1.65±0.34, 3.17±1.03 vs. 1.78±0.37, allP< 0.05). The serum amylase and pancreatic ROS in LPS+ Wortmannin 4 hours group were significantly higher than those of the LPS group at the same time points (U/L: 3 672.00±779.24 vs. 2 432.20±442.85, kU/L: 3.14±0.98 vs. 1.87±0.42, both P< 0.05), but there were no differences in above two parameters between LPS+ Mito Q 6 hours group and LPS group (U/L: 2 975.20±687.03 vs. 2 881.00±550.12, kU/L: 3.17±1.03 vs. 3.18±1.06, bothP> 0.05). Light microscopy showed that obvious pathological changes were found in the pancreas in the LPS 6 hours and 12 hours groups, LPS+Wortmannin 4 hours group, and LPS+ Mito Q 6 hours group. Electron microscopy showed that the number of autophagic vacuoles increased 6 hours after LPS administration. There was no difference at any time point in the number of autophagic vacuoles between LPS+ Mito Q 6 hours group and LPS 6 hours group, and the autophagic vacuoles were not found after Wortmannin intervention. It was demonstrated by Western Blot that the levels of LC3 protein in the LPS 6 hours and 12 hours groups, and LPS+ Mito Q 6 hours group were significantly higher than those of the control group at the same time points (A value: 0.34±0.02 vs. 0.17±0.02, 0.37±0.03 vs. 0.18±0.04, 0.36±0.02 vs. 0.17±0.02, allP< 0.05), but there were no differences between LPS 12 hours group or LPS+ Mito Q 6 hours group and LPS 6 hours group (bothP> 0.05).Conclusions Autophagy prevents exocrine dysfunction of pancreas in septic rats, and the autophagic capacity or autophagosome-formation rate may determine the development of exocrine pancreatic dysfunction. The mitochondria-targeted antioxidant Mito Q does not prevent exocrine dysfunction of pancreas.

Objective To investigate the effects of autophagy on cardiac function and to determine whether the mitochondrial coenzyme Q (MitoQ) prevents cardiac dysfunction,mediated by autophagy,in rats with acute sepsis.Methods Forty-five Sprague Dawley (SD) rats were randomly divided into 9 groups (n =5,each group):control group,4 h lipopolysaccharide(LPS) group,6 h LPS group,12 h LPS group,4 h LPS + Wortmannin group,4 h LPS + MitoQ group,6 h LPS + MitoQ group,MitoQ group and Wortmannin group.Rats in LPS + Wortmannin group and LPS + MitoQ group were intraperitoneally given LPS(10 mg/kg) and followed by an injection of Wortmannin(2 mg/kg) and MitoQ (6.5 μmol/kg) via tail vein 1 hour later,respectively.Rats in each group were given the same amount of normal sodium in addition to different intervention drugs.The cardiac function parameters were measured by a BL-420E + biosignal collection system.Blood samples from abdominal aorta were taken at each time point,and creatine kinase MB isoenzyme (CK-MB) content was detected by using the velocity method.The content of reactive oxygen species (ROS) in isolated myocardial tissues in rats was measured by enzyme-linked immunoadsorbent assay(ELISA).The protein expression of microtubule-associated protein 1 light chain 3 (LC3) was detected by Western blot method.The pathological changes of myocardial tissue were observed by light and electronic microscopy.Results Compared with the control group,the left ventricular systolic pressure(LVSP),the rate of the rise in left ventricular pressure (± dp/dt max) were significantly decreased in 6 h LPS group,6 h LPS + MitoQ group and 4 h LPS + Wortmannin group(P ＜0.05),left ventricular end-diastolic pressure(LVEDP) was significantly increased in these 3 groups(P ＜0.05).The contents of CKMB and ROS in 6 h LPS group,6 h LPS =MitoQ group and 4 h LPS + Wortmannin group were higher than those in the control group(P ＜ 0.05).Electron microscopy showed that the number of autophagic vacuoles increased 6 h after LPS was administered,but did not increase significantly thereafter to 12 h.There was no difference at any time point in the number of autophagic vacuoles in the group given MitoQ and LPS.Immunoblotting demonstrated that the levels of LC3Ⅱ protein in the LPS 6 h group and LPS + MitoQ 6 h group were higher than those in the control group(P ＜0.05),but there was no difference between the LPS 12 h and LPS 6 h groups (P ＞ 0.05).Conclusions The mitochondria-targeted antioxidant MitoQ does not prevent cardiac dysfunction.However,autophagy prevents cardiac dysfunction,and the autophagic capacity or autophagosome-formation rate may determine whether cardiac dysfunction develops.

Objective To investigate the protective effects and mechanism of insulin(INS) on brain in septic rats,and explore the possible role of uncoupling protein 2 (UCP2) in these effects.Methods Fifty male specific pathogen free(SPF) Sprague-Dawley rats were randomly divided into normal control (CN) group(n=10),lipopolysaccharide(LPS) group(n=20) and INS group (n=20) according to random number table.The septic rat model was established through an intraperitoneal injection of 15 mg/kg LPS of gram-negative bacteria.The rats in the INS group received a 1 U/kg INS injection subcutaneously 30 minutes before the injection of LPS,and the rats in the CN group were given equivalent 9 g/L saline in the same way.Eight rats in each group were killed,and their cerebral cortex were collected after the injection of LPS for 24 h.Pathological change of cerebral cortex was detected by Hematoxylin-Eosin(HE) staining.The cerebral cortex mitochondia were extracted for detecting the levels of reactive oxygen species(ROS),malondialdehyde (MDA) and the activity of superoxide dismutase(SOD).Neuronal apoptosis was detected by terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling staining.UCP2 mRNA expression was detected by quantitative real-time(RT)-PCR.Apoptosis-associated protein B lymphocyte tumor-2(Bcl-2),Bcl-2 associated X protein(Bax),cleaved cysteinyl aspartate specific protease(cleaved Caspase-9) and UCP2 protein expression were determined by Western blot.Results (1)Compared with the CN group,obvious abnormal pathological change was revealed by HE staining in cerebral cortex of rats in the LPS group and the INS group,but the pathological change was attenuated in the INS group compared with the LPS group.(2)Compared with the CN group,the levels of mitochondrial ROS[(210.01±14.09) RFU vs.(49.06±7.28) RFU] and MDA[(2.19±0.18) nmol/mg pro vs.(1.25±0.11)nmol/mg pro]in the LPS group significantly increased,whereas SOD activity significantly decreased [(238.49±35.60) U/g pro vs.(446.66±24.90)U/g pro],and the differences were significant(all P<0.05).Compared with the LPS group,the levels of ROS [(152.69±15.83) RFU vs.(210.01±14.09) RFU] and MDA[(1.55±0.14) nmol/mg pro vs.(2.19±0.18) nmol/mg pro] in the INS group decreased,while SOD activity increased[(327.8±23.26) U/g pro vs.(238.49± 35.60) U/g pro],and the differences were significant(all P<0.05).(3)Compared with the CN group,the neuronal apoptosis index of cortex in the LPS group was elevated[(54.16±6.84)% vs.(5.45±1.43)%],while the expression of Bcl-2 decreased (627±0.018 vs.0.739±0.020),but the expressions of Bax(0.768±0.019 vs.0.520±0.010) and cleaved Caspase-9(0.739±0.016 vs.0.467±0.030) increased,and the differences were significant(all P<0.05).Compared with the LPS group,the neuronal apoptosis index of cortex in the INS group decreased [(33.30±3.07)% vs.(54.16±6.84)%],but the Bcl-2 expression increased (0.743±0.022 vs.0.627±0.018),and Bax (0.687±0.034 vs.0.768±0.019) and cleaved Caspase-9(0.551±0.013 vs.0.739±0.016) were reduced,and the differences were significant (all P<0.05).(4)Compared with the CN group,the mRNA (2.248±0.155 vs.1.000±0.100) and protein expression of UCP2 (0.659±0.016 vs.0.599±0.018) were elevated in the LPS group.Compared with the LPS group,the UCP2 mRNA (2.944±0.117 vs.2.248±0.155) and UCP2 protein (0.719±0.018 vs.0.659±0.016) increased,and the differences were significant(all P<0.05).Conclusions INS can protect the brain of septic rats through alleviating mitochondrial oxidative stress and inhibiting the mitochondrial-initiated apoptotic pathway to reduce neuronal apoptosis.INS upregulates UCP2 expression in the brain of septic rats,which may play a role in the protective effects mentioned above.

Objective To investigate the protective effect of continuous intravenous infusion of Isoproterenol (ISO)on myocardial mitochondria of early septic rats and the corresponding mechanism.Methods Thirty Sprague Dawley (SD)rats were randomly divided into 5 groups (6 cases per group):control group,endotoxin group,ISO small-dose group,ISO medium-dose group and ISO large-dose group.Endotoxin group and ISO intervene group received same management apart from drug intervention:receiving intravenous injection of lipopolysaccharide (LPS)10 mg/kg followed by an continuous intravenous infusion of 9 g/L saline 1 mL/h or ISO 0.06 μg/(kg · min),0.30 μg/(kg · min)and 0.60 μg/(kg · min).Control group received intraperitoneal injection and continuous intravenous infusion with the same amount of 9 g/L saline.The primary endpoint of the study was 24 hours after injection of 9 g/L saline or LPS.Serum creatine kinase (CK) and creatine kinase isoenzyme (CK-MB),oxidative and nitrosative stress levels and swelling of isolated heart mitochondrion were detected.The pathological changes of the myocardium and morphologic changes of the heart mitochondria were observed through light microscope and scanning electron microscope,respectively.Results The levels of CK,CK-MB,nitric oxide (NO) content,inducible nitric oxide synthase (iNOS) activity and malondialdehyde (MDA)content in endotoxin group were increased compared with control group (all P ＜ 0.05),while the superoxide dismutase (SOD) activity decreased [(11.543 ± 1.080) U/mg prot vs (9.892 ±0.815) U/mg prot,P ＜0.05].The morphology of the heart mitochondria significantly changed (such as swelling,disordered arrangement,crest fracture,fusion and cavitations,and so on).ISO intervention significantly decreased the levels of CK,CK-MB and mitochondrial swelling (all P ＜ 0.05) and increased the SOD activity (all P ＜ 0.05).The levels of NO content,iNOS activity and MDA content were significantly decreased in small-dose group [(10.823 ± 2.240) μmol/g prot vs (7.917 ± 2.203) μmol/g prot,(0.045 ± 0.008) U/mg prot vs (0.033 ± 0.003) U/mg prot,(1.663 ± 0.618) mmol/mg prot vs (0.768 ± 0.312) mmol/mg prot,all P ＜ 0.05],while the levels of iNOS activity and MDA content were significantly increased in medium-and large-dose group (all P ＜ 0.05) ; compared with medium-dose group,the degree of mitochondrial swelling in large-dose group increased (1.160 ± 0.186 vs 1.393 ± 0.128,P ＜ 0.05).The pathological changes of the myocardium mitochondria significantly improved.Conclusions The myocardium and myocardial mitochondria of early septic rats were damaged,continuous intravenous infusion of low-dose ISO revealed protective effect on these damages,and the corresponding mechanism may relate to the decrease of the oxidative and nitrosative stress.

Objective To investigate the differential expression of microRNA - 30e in sepsis - induced acute lung injury(ALI)and its correlation with interleukin(IL)- 1β and tumor necrosis factor(TNF)- α from two aspects of in vivo and in vitro. Methods Thirty SD male rats were randomly divided into 5 groups:normal control group,3 - hour sepsis group,6 - hour sepsis group,12 - hour sepsis group and 24 - hour sepsis group in equal number. Sepsis - in-duced ALI model was induced by intraperitoneal injection of lipopolysaccharide(LPS,10 mg/ kg). The rat alveolar mac-rophages NR8383 were divided into blank control group and LPS(1 mg/ L)stimulated 3,6,12,24 hour groups. Inverse transcription - polymerase chain reaction was used to assay the production changes of IL - 1β,TNF - α and miRNA - 30e in lungs and cells. The injury of lung tissue was evaluated through histopathology. Results The levels of IL - 1β and TNF - α in lung tissues of rats in sepsis groups were obviously up - regulated when compared with those in normal control groups(all P ﹤ 0. 01). The lung tissue hematoxylin - eosin staining indicated ALI in the sepsis group. The relative expression of miR - 30e in rat lung tissue in sepsis 3,6,12,24 hour groups were respectively 0. 26 ± 0. 02, 0. 41 ± 0. 08,0. 29 ± 0. 05 and 0. 18 ± 0. 05,which were significantly lower than those in normal control group(1. 23 ± 0. 24,all P ﹤ 0. 01). The levels of IL - 1β and TNF - α in LPS stimulated NR8383 cells at different time points were obviously up - regulated when compared with those in blank control groups(all P ﹤ 0. 01). The relative expression of miR - 30e in LPS stimulated 3,6,12,24 hour groups were respectively 0. 27 ± 0. 04,0. 55 ± 0. 05,0. 65 ± 0. 02 and 0. 41 ± 0. 10,which were significantly lower than those in blank control group(1. 17 ± 0. 21,all P ﹤ 0. 01). The expres-sion of miR - 30e in lung tissues of groups showed significantly negative correlations with those of IL - 1β and TNF - α(IL - 1β:r = - 0. 417,P = 0. 022;TNF - α:r = - 0. 437,P = 0. 016). The expression of miR - 30e in LPS stimulated NR8383 cells of groups also showed significantly negative correlations with those of IL - 1β and TNF - α(IL - 1β :r =- 0. 713,P = 0. 003;TNF - α:r = - 0. 712,P = 0. 002). Conclusions The expression level of miR - 30e was signifi-cantly down - regulated in sepsis - induced ALI,and had a significantly negative correlation with IL - 1β and TNF - α, which may be used as a new biomarker of diagnostic,prognosis evaluation and therapy of sepsis - induced ALI.

Objective To invkstigatk thk kffkcts of intkrlkucin-6(IF-6)on mitochondrial biogknksis in ac-tivatkd astrocetks(LS)and thk rolk of adknosink monophosphatk protkin cinask( LMPK)in this prockss. Methods Thk LS isolatkd from nkonatal rat ckrkbral codkx wkrk purifikd and culturkd. Thk LS was randomle dividkd into 5 groups:control group,lipopolesaccharidk(FPS)+intkrfkron-γ(IPN-γ)group( IPN-γ group),FPS+IPN-γ+IF-6 group(IF-6 group),FPS+IPN-γ+IF-6A siANL+IF-6 group(siANL group),and FPS+IPN-γ+nkga-tivk control(NC)+IF-6 group(NC group),thkn,LS in kach group was trkatkd for 6 h. Tumor nkcrosis factor-α (TNP-α)mANL and intkrlkucin-1β(IF-1β)mANL kxprkssion wkrk dktkctkd be adopting rkvkrsk transcription-polemkrask chain rkaction(AT-PCA). Thk lkvkls of rkactivk oxegkn spkciks(AOS)wkrk dktkctkd be fluorksknt probk mkthod and thk lkvkls of adknosink triphosphatk(LTP)wkrk dktkctkd be lucifkrask mkthod. Ckll viabilite was kvaluatkd be using ckll count Kit-8. Pkroxisomk prolifkrator-activatkd rkckptor gamma coactivator-1α(PGC-1α),nuclkar rk-spiratore factor-1(NAP-1),mitochondrial transcription factor L( TPLM)and phospho-adknosink monophosphatk activatkd protkin cinask(p-LMPK)protkin kxprkssion wkrk dktkctkd be using Zkstkrn blotting. ResuIts (1)Com-parkd with thk control group,thk mANL kxprkssions of TNP-α and IF-1β(2. 548 ± 0. 154 vs. 1. 000 ± 0. 001,P﹦ 0. 000;2. 912 ± 0. 102 vs. 1. 000 ± 0. 001,P﹦0. 000),thk lkvkls of AOS[(245. 307 ± 13. 379)APR vs.(69. 460 ± 7. 257)APR,P﹦0. 000]and LTP[(1. 558 ± 0. 008)nmol╱mg protkin vs.(1. 016 ± 0. 025)nmol╱mg protkin,P﹦0. 000]significantle klkvatkd,and thk ckll viabilite(0. 840 ± 0. 013 vs. 1. 000 ± 0. 001,P﹦0. 000)dkcrkaskd,whilk thk protkin kxprkssion of NAP-1(0. 406 ± 0. 045 vs. 0. 157 ± 0. 016,P﹦0. 017),TPLM(0. 605 ± 0. 025 vs. 0. 416 ± 0. 013,P﹦0. 005)klkvatkd in FPS+IPN-γ group,and thk diffkrkncks wkrk significant(all P＜0. 05).(2)Comparkd with FPS+IPN-γ group,thk lkvkls of LTP[(1. 763 ± 0. 028)nmol╱mg protkin vs.(1. 558 ± 0. 008)nmol╱mg pro-tkin,P﹦0. 000],thk ckll viabilite(0. 910 ± 0. 024 vs. 0. 840 ± 0. 013,P﹦0. 008)wkrk klkvatkd,whilk thk protkin kx-prkssion of PGC-1α(0. 724 ± 0. 027 vs. 0. 586 ± 0. 039,P﹦0. 000),NAP-1(1. 036 ± 0. 211 vs. 0. 406 ± 0. 045,P﹦0. 000),TPLM(0. 786 ± 0. 058 vs. 0. 605 ± 0. 025,P﹦0. 002)and p-LMPK(1. 094 ± 0. 223 vs. 0. 755 ± 0. 084,P﹦0. 014)wkrk klkvatkd in IF-6 group,and thk diffkrkncks wkrk significant( all P＜0. 05).(3)Comparkd with IF-6 group,LTP[(1. 187 ± 0. 005)nmol╱mg protkin vs.(1. 763 ± 0. 028)nmol╱mg protkin,P﹦0. 000]and thk ckll viabili-te(0. 680 ± 0. 040 vs. 0. 910 ± 0. 024,P ﹦0. 000)all dkcrkaskd in siANL group,whilk thk protkin kxprkssion of PGC-1α(0. 631 ± 0. 022 vs. 0. 724 ± 0. 027,P﹦0. 020),NAP-1(0. 386 ± 0. 066 vs. 1. 036 ± 0. 211,P﹦0. 000), TPLM(0. 593 ± 0. 022 vs. 0. 786 ± 0. 058,P﹦0. 009)and p-LMPK(0. 365 ± 0. 063 vs. 1. 094 ± 0. 223,P﹦0. 002) significantle dkcrkaskd in siANL group,and thk diffkrkncks wkrk significant(all P＜0. 05). ConcIusions IF-6 can incrkask mitochondrial biogknksis in activatkd LS,which is probable mkdiatkd through up-rkgulating thk kxprkssion of LMPK.

Objective To preliminarily investigate the role of Vitamin C in cecal ligation and puncture-induced septic brain injury.Methods Male specific pathogen free (SPF) Sprague-Dawley male rats were randomly assigned into control group,sham operation group,sepsis group and sepsis therapy group.The rats in sepsis group were prepared by cecal ligation and puncture.The rats in sepsis therapy group were injected sodium ascorbate through the tail vein 3 h after the cecal ligation and punature procedure.The animals in other groups were subjected only to subcutaneous bolus injection of 9 g/L saline only.Animals were evaluated by neurologic reflex scores before sacrifice and brain tissues were quickly removed at the indicated time points.Reactive oxygen species (ROS),superoxide dismutase (SOD),malondialdehyde (MDA),nitric oxide (NO),inducible nitric oxide synthase (iNOS) and catalase (CAT) were determined by using enzyme assay kits.Hematoxylin-eosin (HE) staining was used to observe morphological changes in brain tissues.Results The survival rate of the sepsis group (30％ at 7th day) was significantly lower than that of the control group (100％ at 7th day)and sham operation group(100％ at 7th day).The survival rate of the sepsis therapy group (45％ at 7th day)was significantly higher than that of the sepsis group(P ＜ O.05).The neurological reflex assessment began to decrease at 6 h in sepsis group and reached the lowest at 24 h (6.00 ± 0.53).The sepsis therapy group (7.62 ± 0.52) was significantly higher (P ＜ 0.05) than the sepsis group and began to recover at 72 h (8.63 ±0.52).ROS,SOD,MDA,NO and iNOS in the sepsis group and the sepsis therapy group reached a peak at 24 h,which decreased at 72 h.The value in sepsis therapy group was significantly decreased than that in the sepsis group,and the difference was statistically significant(P ＜0.05).CAT changed in the opposition.The SOD/CAT in sepsis group was the highest 24 h after the operation,while the ratio in sepsis therapy group was significantly improved.SOD/CAT and MDA were positively correlated(r =0.968,P ＜ 0.05).HE staining showed significant damage to the brain tissue structure in the sepsis group,however some improvement was observed in the sepsis therapy group.Conclusion Vitamin C can significantly improve the survival rate and encephalopathy prognosis in the cecal ligation and puncture SD rat models.The mechanism may be related to the reduction of oxidative stress.