Objective To study the effect of PGE_1 injection on hepatorenal syndrome.Methods 64 patients with hepatorenal syndrome were divided into two groups at random,33 cases in treatment group and 31 cases in control group.On the basis of complex treatment of the contrast group were added PGE_1 of 200?g,dissolved at 10% glucose liquid 100ml,ivgtt,qd,the course of treatment is 2 weeks.Results The improvement which treated the liver function of the group was superior to the contrast group(P

Objective To probe into the serum blood platelet and turn into the plain(TPO) dependence that the blood platelet of level, liver cell function and periphery counts in purpose. Methods Among 106 cases of virus hepatitis patients in hsopital measuring, serum TPO level was carried on with ELISA. According to having blood platelet to reduce and divide into: A, B,C,D,E,F, G.H, group I. Results Between group A and group B,group C and group D,group E and group F,group G and group H,serum TPO level had significant differences(P

Objective To investigate the relationship between serum HBV.M.alanine transaminase(ALT) and hepatic tissue pathology in patients with chronic hepatitis B.Methods The serum HBV.M.liver function in 133 patients with chronic hepatitis B were measured,and these patients underwent percutaneous liver biopsy by colour Echo.All these patients were divided into eight groups according to HBeAg and HBV DNA positive or negative,ALT normal or not.Hepatic necrosis inflammation grade and hepatic fibrosis stage in the groups were compared.Results Hepatic histology of all these patients showed inflammation and necrosis and different degree fibrosis.In serum ALT normal patients,liver biopsy still showed different degrees inflammation and hepatic fibrosis degrees partly,even showed hepatocirrhosis.In serum ALT abnormal and HBeAg negative patients with chronic hepatitis B patients,hepatic tissue inflammation and fibrosis degrees were more serious,hepatic tissue pathology was out of proportion to the degree of serum HBV reproduction.Conclusion Judgment of disease activity doesn't only depend on the serum transaminases and the degree of serum HBV DNA replication.When clinical choosing indication of antiviral therapy,value of liver biopsy should not be substituted.Liver biopsy in chronic hepatitis B should be regarded as main basis of judgment the hepatitis activity.It also should be regarded as main basis if antiviral therapy is conducted.

Objective To explore the significance of blood coagulation disorder in acute pancreatitis(AP) of the elderly and its treatment with prostaglandin E_1.Methods Prothrombin time(PT),partially activated thromboplastin time(APTT) and fibrinogen(FIB) in cases of AP with ages over 60 were checked and compared with those in groups of AP with ages under 60 and normal control subjects.10 cases of AP of the elderly with elevated FIB were treated with prostaglandin E_1.Results Compared with groups of AP with ages under 60 and the normal subjects,FIB was significantly higher in cases of AP of the elderly with the highest in patients of SAP.8 out of 10 aged AP patients with elevated FIB was successfully treated with prostaglandin E_1.Conclusion Patients of AP may present with blood coagulation disorders especially in aged patients.Aged patients with elevated fibrinogen may predispose to SAP.Prostaglandin E_1 may be effective in this occasion.

Objective:To evaluate the effects of intranasal administration of glial cell line-derived neurotrophic factor (GDNF) on postoperative cognitive dysfunction in aged rats.Methods:Forty healthy Sprague-Dawley rats of both sexes, aged 21-23 months, weighing 480-600 g, were divided into 4 groups ( n=10 each) using a random number table method: sham operation group (group S), operation group (group O), intranasal administration of low-dose GDNF group (group G1) and intranasal administration of high-dose GDNF group (group G2). Rats underwent exploratory laparotomy under anesthesia with chloral hydrate in O, G1 and G2 groups, while the rats in group S only received sham operation.The rats in group G1 and group G2 were intranasally treated with GDNF 25 and 50 μg (in 25 μl of PBS), respectively, and PBS 25 μl was nasally administered in group S and group O every day for 3 consecutive days after operation or sham operation.Morris water maze test was performed on days 3-7 after surgery, and then the rats were sacrificed, and hippocampal tissues were removed for determination of the expression of GDNF, high mobility group box 1 (HMGB1), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), activated caspase-3 and Bax (by Western blot). Results:Compared with group S, the escape latency was significantly prolonged on days 5-7 after operation, the number of crossing the platform was reduced, time spent in the target quadrant was shortened, expression of GDNF was down-regulated, and expression of IL-1β, TNF-α, HMGB1, activated caspase-3 and Bax in hippocampi was up-regulated in group O, and the number of crossing the platform was reduced, time spent in the target quadrant was shortened, and expression of IL-1β and TNF-α was up-regulated in G1 and G2 groups ( P<0.05). Compared with group O, the escape latency was significantly shortened on days 5-7 after operation, the number of crossing the platform was increased, time spent in the target quadrant was prolonged, expression of GDNF was up-regulated, expression of TNF-α, HMGB1, activated caspase-3 and Bax in hippocampi was down-regulated in G1 and G2 groups, and IL-1β in hippocampi was down-regulated in group G1 ( P<0.05). Compared with group G1, the expression of TNF-α in hippocampi was down-regulated ( P<0.05), and no significant change was found in the other parameters mentioned above in group G2 ( P>0.05). Conclusions:Intranasal administration of GDNF can improve postoperative cognitive dysfunction, and the mechanism may be related to inhibiting neuroinflammatory responses and neuroapoptosis in aged rats.

Objective To investigate the effects of intrathecal dexmedetomidine administration on the development of morphine tolerance and spinal inflammatory responses.Methods Thirty-three male SD rats weighing 180～200 g were randomly divided into 3 groups (n=11):Saline group (group NS),Morphine group (group M) and Dexmedetomidine group (group Dex).Animals of group NS were intrathecally injected with 10 tμL of saline daily for seven days;Animals in group M were intrathecally injected with 15 μg of morphine daily for seven days;Animals in group Dex were intrathecally injected with a mixture of 15μg morphine and 1.5 μg dexmedetomidine daily for seven days.At 1,3,5 and 7 day of intrathecal injection,hot water tail-flick test were used to evaluate analgesic response to thermal stimuli.After the last episode of behavioral test,Western blot analysis was applied to determine the protein levels of Iba-1 (microglial marker),IL-1β,TNF-a and phospho-p38MAPK (p-p38) in the spinal cord.In addition,microglia in the spinal cord was immuno-stained with anti-Iba-1 antibody and the densities of microglia were calculated.Results In group M and Dex,the values of maximal possible effect (MPE) in tail-flick test decreased gradually along with repeated morphine administration (P＜0.05).Compared with group NS,the values of MPE in tail-flick test at 1,3,5 and 7 day of morphine tolerance were higher in group M (P＜0.05).Compared with group M,the values of MPE in tail-flick test at 3,5 and 7 day of morphine tolerance were higher in group Dex (P＜0.05).Compared with group NS,the spinal protein levels of Iba-1,IL-1L TNF-α and p-p38 as well as the density of Iba-1 positive cells in group M were increased (P＜0.05).However,Compared with group M,the of Iba-1,IL-1β,TNF-α and p-p38 as well as the density of Iba-1 positive cells were decreased(P＜0.05).Conclusion Intrathecal dexmedetomidine administration can attenuate morphine tolerance by inhibiting microglia-mediated inflammatory responses in the spinal cord.

Objective To investigate the role of transient receptor potential melastatin 7(TRPM7) in sevoflurane preconditioning for inhibiting hippocampal neurons apoptosis and inflammation response induced by oxygen-glucose deprivation(OGD).Methods Fifty SD rats of postnatal 1 d were selected for extracting hippocampal neurons and randomly divided into 5 groups,including the control group(C),sevoflurane preconditioning group (Sev),OGD group,Sev preconditioningt OGD group (Sev + OGD) and Sev preconditioning+ bradykinin+OGD group(combined group).After 1.5 h oxygen-glucose deprivation,reintroduction was performed,and then the normal culture was performed again for preparing the OGD model.Hippocampal neurons in the control group were normally cultured only;which in the Sev group conducted 2 ％ Sev preconditioning for 1 h;which in the OGD group only prepared the OGD model;which in the SEv+OGD conducted 2％ Sev preconditioning for 1 h,and prepared the OGD model after 24 h;which in the combined group was simultaneously added with bradykinin(final concentration 200μmol/L) in Sev preconditioning,other treatment was same to that in the Sev+OGD group.After 24 h normal culture,the mRNA and protein levels of TRPM7,apoptosis rate,survival rate,mRNA and supernatant protein levels of IL-1β and TNF-α of the hippocampal neurons were detected.Results Compared with the control group,hippocampal neurons mRNA and protein levels of TRPM7,apoptosis rate,mRNA and supernatant protein levels of IL-1β and TNF-α in the OGD group were significantly increased(P＜0.05),whereas the survival rate was significantly decreased (P ＜ 0.05).Compared with the OGD group,hippocampal neurons mRNA and protein levels of TRPM7,apoptosis rate,mRNA and supernatant protein levels of IL-1β and TNF-α in the Sev group were significantly decreased(P＜0.05),whereas the survival rate was significantly increased(P＜0.05).Compared with the Sev group,hippocampal neurons mRNA and protein levels of TRPM7,apoptosis rate,the mRNA and supernatant protein levels of IL-1β and TNF-α in the combined group were significantly increased(P＜0.05),whereas the survival rate was significantly decreased(P＜0.05).Conclusion Sev preconditioning can attenuate hippocampal neurons apoptosis and inflammatory response after OGD via alleviating the overexpression of TRPM7.

Objective To evaluate the role of nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in remote ischemic preconditioning-induced reduction of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.Methods Sixty-eight healthy male C57BL/6 mice,aged 6-8 weeks,weighing 22-26 g,were divided into 4 groups (n =17 each) using a random number table:control group (group C),ALI group,remote ischemic preconditioning group (group RIPC) and brusatol plus remote ischemic preconditioning group (group B+RIPC).Normal saline 100 μl was intratracheally instilled in group C.ALI was induced by intratracheal instillation of LPS 5 mg/kg in group ALI.Mice in group RIPC were subjected to 6 cycles of 5-min ischemia followed by 5-min reperfusion in the right hindlimbs using a tourniquet,and 1 h later the model of ALI was established.Nrf2 inhibitor brusatol 2 mg/kg (in 100 μl of 1％ dimethyl sulfoxide) was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model in group B.Brusatol 2 mg/kg was intraperitoneally injected every other day for 10 days prior to establishment of the ALI model,and remote ischemic preconditioning was performed at 1 h before establishment of the ALI model in group B+RIPC.Seven mice in each group were selected at 24 h after establishment of the ALI model,and bronchoalveolar lavage fluid (BALF) was collected for determination of protein concentrations and neutrophil count.Mice were then sacrificed and lungs were removed for determination of lung water content,myeloperoxidase (MPO) activity,contents of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α),and expression of Nrf2,HO-1 and high-mobility group box 1 protein (HMGB1) in lung tissues (by Western blot) and for examination of pathological changes (with a light microscope).Results Compared with group C,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,and the expression of Nrf2,HO-1 and HMGB1 was up-regulated in group ALI (P＜ 0.05).Compared with group ALI,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly decreased,the expression of Nrf2 and HO-1 was up-regulated,and the expression of HMGB1 was down-regulated (P＜0.05),and the pathological changes were significantly attenuated in group RIPC.Compared with group RIPC,the lung water content,MPO activity,contents of IL-1β and TNF-α,and neutrophil count and protein concentrations in BALF were significantly increased,the expression of Nrf2 and HO-1 was down-regulated,and the expression of HMGB1 was up-regulated (P＜0.05),and the pathological changes were aggravated in group B+RIPC.Conclusion The activation of Nrf2/HO-1 signaling pathway is involved in remote ischemic preconditioning-induced reduction of LPS-induced ALI in mice.

Objective To evaluate the relationship between α7 nicotinic acetylcholine receptor (α7nAChR) signaling pathway and regulatory T cells (Tregs) during vagus nerve stimulation-induced reduction of endotoxin-caused acute lung injury (ALI) in mice.Methods Clean-grade healthy male C57BL/6 mice,aged 6-8 weeks,weighing 22-25 g,were divided into 5 groups (n=10 each) using a random number table method:control group (group C),group ALI,vagus nerve stimulation group (group VNS),α-BGT group (group α-BGT) and vagus nerve stimulation plus α-BGT group (group VNS + α-BGT).After successful establishment of the model,the vagus nerve was stimulated for 30 s with a stimulus intensity of 0.5 mA,frequency of 20 Hz,an interval of 5 min,60 min in total.Sterile normal saline 100 μl was injected into the trachea,and the vagus nerve was only exposed but not stimulated in group C.In group ALI,the ALI model was established,and the vagus nerve was isolated but not stimulated.In group α-BGT,α-BGT 1 μg/kg was intraperitoneally injected,the ALI model was established 1 h later,and the vagus nerve was isolated but not stimulated.In group VNS+α-BGT,α-BGT 1 μg/kg was intraperitoneally injected,the ALI model was established 1 h later,and the vagus nerve was stimulated at 1 h after the end of establishment.Animals were sacrificed at 72 h after establishing the model,and lungs were removed for determination of lung water content,percentage of Tregs (using flow cytometry),myeloperoxidase (MPO) activity (by colorimetric assay),expression of α7nAChR (by Western blot) and contents of interleukin-10 (IL-10),transforming growth factor-β (TGF-β) and IL-1β (by enzyme-linked immunosorbent assay).Results Compared with group C,the lung water content,MPO activity and IL-1β content were significantly increased in the other four groups,the expression of α7nAChR was significantly down-regulated in ALI,α-BGT and VNS+α-BGT groups,the percentage of Tregs was significantly increased in group VNS,the IL-10 content was significantly decreased in ALI and α-BGT groups and increased in VNS and VNS+α-BGT groups,and TGF-β contents were significantly decreased in ALI,α-BGT and VNS+α-BGT groups and increased in group VNS (P＜0.05).Compared with group ALI,the lung water content,MPO activity and IL-1β content were significantly decreased,the expression of α7nAChR was up-regulated,and the percentage of Tregs and contents of IL-10 and TGF-β were increased in group VNS,and the TGF-β content in group α-BGT and contents of IL-10 and TGF-β in group VNS+α-BGT were significantly increased (P＜0.05).Compared with group VNS,the lung water content,MPO activity and IL-1β content were significantly increased,the expression of α7nAChR was down-regulated,and the percentage of Tregs and contents of IL-10 and TGF-β were decreased in α-BGT and VNS+α-BGT groups (P＜0.05).The contents of IL-1O and TGF-β were significantly higher in group VNS+α-BGT than in group α-BGT (P＜0.05).Conclusion Vagus nerve stimulation can activate α7nAChR signaling pathway and raise the percentage of Tregs,thus reducing ALI in mice.

Objective:To evaluate the effect of glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide receptor agonist DA-JC4 on postoperative neuroinflammatory responses in aged rats.Methods:Forty-five Sprague-Dawley rats, aged 21-23 months, weighing 530-630 g, provided by the Animal Experiment Center of Medical School of Zhengzhou University, were assigned into 3 groups ( n=15 each) using a random number table method: sham operation group (group S), operation group (group O) and DA-JC4 group (group G). Rats underwent exploratory laparotomy under anesthesia with chloral hydrate in O and G groups.In group G, DA-JC4 10 nmol/kg (dissolved in 1 ml of sterile normal saline) was intraperitoneally injected immediately after the end of operation and at 24 and 48 h after operation.Western blot was used to determine the expression of hippocampal Bax, Bcl-2, activated caspase-3, Beclin-1, microtubule-associated protein 1 light chain 3Ⅱ (LC3Ⅱ), high-mobility group box 1 protein (HMGB1), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) on day 3 after surgery.The Morris water maze test was performed on days 14-18 after operation to assess the cognitive function. Results:Compared with group S, the escape latency was significantly prolonged on days 15-18 after operation in group O and on day 18 after operation in group G, and the number of crossing the original platform was reduced, the time spent in the target quadrant was shortened, the expression of activated caspase-3, Bax, LC3Ⅱ, HMGB1, IL-1β and TNF-α in hippocampi was up-regulated, and the expression of Bcl-2, LC3Ⅱ and Beclin-1 was down-regulated in O and G groups ( P<0.05). Compared with group O, the escape latency was significantly shortened, and the number of crossing the original platform was increased, the time spent in the target quadrant was prolonged, the expression of activated caspase-3, Bax, LC3Ⅱ, HMGB1, IL-1β and TNF-α in hippocampi was down-regulated, and the expression of Bcl-2, LC3Ⅱ and Beclin-1 was up-regulated in group G ( P<0.05). Conclusion:The mechanism by which DA-JC4 reduces postoperative cognitive dysfunction may be related to inhibiting neuroinflammatory responses in aged rats.