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Objective To explore whether the IL-6/STAT3 signaling pathway regulate the expression of high mobility group proteins1 (HMGB1) in intestinal mucosa of rats with sepsis through the cecum ligation puncture (CLP). Methods One hundred and twenty male SD rats were randomly(random number) divided into three groups: sham operation group (group S, n=40), CLP group(group C, n=40) and anti-IL-6 monoclonal antibody group (group T, n=40). Rats in group S only received the simple laparotomy;Rats in group C and group T were established as a rat model of sepsis using CLP; rats in group T received the intraperitoneal injection of anti-IL-6 monoclonal antibody at 1 h after CLP, while the same volume of sodium lactate ringer's solution was injected to rats in group S and group C. Ten rats in each group were sacrificed at 3, 12, 24 and 48 h, respectively, and intestinal mucosa specimens were collected for pathological examinations by HE staining. The protein expression of HMGB1 and IL-6 were detected by immunohistochemistry, STAT3-protein by Western blot.and the levels of diamine oxidase (DAO) and D lactic acid in plasma by spectrophotometric. Results Rats in group C and group T showed obvious intestinal damage to different degrees, significantly higher intestinal mucosa pathological scores and plasma levels of DAO and D-lactic acid compared with rats in group S (P<0.05). The protein expression of IL-6, HMGBl and p-STAT3 of intestinal mucosa in group C and group T also significantly increased compared with that in group S (P<0.05). The intestinal mucosa pathological score, plasma levels of DAO and D-lactic acid and protein expression of IL-6, HMGBl and STAT3 were decreased in group T compared with those in group C (P<0.05). The intestinal mucosa pathological scores were positively correlated with the protein expression of IL-6 and HMGB1 at 12, 24, and 48 h, respectively. Conclusions IL-6 and HMGBl were involved in the intestinal injury of septic rats. IL-6/STAT3 signaling pathway could up-regulate the expression of HMGB1 in intestinal mucosa of septic rats.
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Objective:To observe the clinical effect of the combined use of dexmedetomidine and propofol for anesthesia in the elderly patients with painless gastroscopy. Methods:Totally 70 elderly patients with painless gastroscopy were selected and randomly divided into the observation group (35 cases) and the control group (35 cases). The observation group was given dexmedetomidine and propofol for anesthesia, while the control group was given propofol for anesthesia. The anesthesia induction time, the vital signs and recovery time of the patients, intraoperative complications and postoperative adverse reactions were observed and compared between the two groups. Results:The anesthesia induction time of the observation group was shorter than that of the control group (P<0. 01). The mean arterial pressure (MAP) in T2, T3 and T4 stage in the two groups were significantly lower than that in T1 stage (P<0. 05, P<0. 01). The HR in T3 stage and RR in T2 stage in the control group were lower than those in T1 stage (P<0. 05). The RR in T2 stage in the observation group was significantly lower than that in T1 stage (P<0. 05). The MAP in T2 and T3 stage in the observation group was significantly higher than that in the control group (P<0. 01), while that in T4 stage in the observation group was significant-ly lower than that in the control group (P<0. 05). The HR in T3 stage in the observation group was significantly higher than that in the control group (P<0. 05). The incidence of intraoperative complications in the observation group was 5. 7%, while that in the con-trol group was 22. 9%, and there was significant difference between the two groups (P<0. 05). The recovery time in the observation group was shorter than that in the control group (P<0. 01). Conclusion:Dexmedetomidine combined with propofol has better anes-thesia effect and higher safety than propofol alone, which is worthy of clinical promotion.
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[ABSTRACT]AIM:Toexplorethedevelopmentofhepaticsinusoidalcapillarizationintheearlystageofliverfi-brosis induced by carbon tetrachloride (CCl4) in rats.METHODS:Clean SD rats were randomly divided into normal con-trol group (group N, n=6) and liver fibrotic model group (group M, n=32).The rats in group N were intraperitoneal in-jected with saline and the rats in group M were intraperitoneal injected with CCl 4(2 mL/kg, twice a week for 4 weeks).At the end of the 3rd day and the 1st, 2nd and 4th weeks, all rats were killed and then the samples were collected .The patho-logical changes in the livers were observed by HE staining and Masson straining .The development of hepatic sinusoidal capillarization was observed by transmission electron microscopy (TEM) and immunohistochemical staining .The cell sur-face expression of vascular endothelium-associated marker CD31, collagen type Ⅳ(Col IV) and laminin (LN) was deter-mined.RESULTS:HE and Masson staining showed the formation of liver fibrosis after treatment with CCl 4 for 4 weeks. TEM showed that the fenestrate diameter of liver sinusoidal endothelial cells (LSECs) grew down, the fenestrate numbers of LSECs were decreased along with the development of liver fibrosis , and the consecutive basement membrane was formed at the end of the experiment .The expression of CD31 was significantly increased along with the development of defenestration , and the expression of Col IV and LN was significantly increased after the treatment with CCl 4 for 2 weeks and 4 weeks , re-spectively .CONCLUSION:The typical hepatic sinusoidal capillarization was detected in the early stage of liver fibrosis , and the deposition of LN in the liver sinusoidal walls was the mainly factor of formation of the consecutive basement mem -brane .
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Objective:To study the effects of rat interleukin-10 (rIL-10) gene treatment on the expression of collagen , matrix metalloproteinase 13(MMP13) and their specific inhibitors the tissue inhibitor of metalloproteinase 1(TIMP1) in porcine serum in-duced liver fibrosis rats then to explore the anti-fibrotic effect of rL-10.Methods:Thirty SD rats were divided into normal control and fibrosis model group.Normal control group (group C) was intraperitoneally injected with 0.5 ml normal sodium twice a week for 8 week, while the fibrosis model group was injected with equal volume of pig serum for 8 week.At the beginning of the 5th week, fibrosis model group was further randomly divided into a fibrosis model subgroup ( group M ) , rIL-10 gene treatment subgroup ( group I ) and empty vector control subgroup(group P).Rats in group C and M were injected with Ringer’s solution as a reagent control via the tail vein weekly, rats in group I were injected with the rIL-10 plasmid pcDNA3-rIL-10, and rats in group P were injected with empty vector pcDNA3.All rats were sacrificed at the end of 8th week, and the liver tissue samples were collected to observe deposition of collegan in liver tissue by sirius red staining and detected the expression of MMP 13 and TIMP1 in the liver tissue by SP immunohistochemistry .Re-sults:Sirius red staining showed that the area of the collegan deposition was dramatically increased in fibrosis model subgroup and emp -ty vector control subgroup compared with the normal control group , and the area of the collagen deposition was dramatically decreased in rIL-10 gene treatment subgroup compared with the fibrosis model and empty vector control subgroup .Immunohistochemistry analysis showed that the expression of MMP 13 and TIMP1 in fibrosis model subgroup and empty vector control subgroup was significantly higher than the normal control group , but compared with normal control group , expression of MMP13 was significantly increased and expres-sion of TIMP1 was significantly decreased in rIL-10 gene treatment subgroup .Compared with fibrosis model subgroup and empty vector control subgroup, the expression of MMP13 and TIMP1 was dramatically decreased in rIL-10 gene treatment subgroup.Conclusion:rIL-10 gene treatment attenuates the area of collagen deposition in liver fibrosis rats associated with downregulation of TIMP 1.
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Objective To observe the effects and mechanism of pretreatment in rats with prostaglandin E1 on liver after hemorrhagic shock and resuscitation(HSR).Method In total,32 male SD rats were randomly(random number)divided into four groups(n=8):group A(sham group),group B(shock group),group C(HSR group)and group D(Lipo-PGEl+HSR).In group B,rats were sacrificed 90 min after shock,and in group C,rats were anesthetized and then subjected to hemorrhagic shock followed by resuscitation.In group D,rats were pretreated with Lipo-PGEI one hour before HSR.Liver function,NO and ET.1 were measured,and pathological changes of liver tissue in each group were observed,and the expres8ions of iNOS and ET.1 of liver tissue were measured by using immunohistochemistry 6 hours after HSR.Data were analyzed by analysis of variance,and P<0.05 was considered as significantly different in statitistics.Results The levels of liver iNOS and ET-I increased in HSR group compared with shock group [(O.225±0.080)vs.(0.082±0.021)and(0.292±0.047)vs.(0.082±0.035),P<0.05].Pretreatment with Lipo-PGEl markedly reduced the damage of Liver function,and lowered the levels of NO and ET-I.which were consistent with decrease in iNOS and ET-16 hours after HSR[(0.116±0.034)vs.(0.225±0.080)and(0.198±0.041)vs.(0.292±0.047),P<0.05].Conclusions Pretreatment with Lipo-PGEl could reduce liver injury after HSR.The mechanisms might be attributed to inhibiting iNOS and ET-1,regulating the balance of NO/ET-I.
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Aim To establish a method of hydrodynamic-based transfection(HBT) and provide a means in rats of the gene therapy of liver diseases,which allowed an efficient expression of rIL-10 gene in rat liver.Methods Using rIL-10 gene as a reporter gene,different volumes and doses of plasmid DNA solutions were rapidly injected into rat tail vein,then the serum and the tissue of liver,kidney,lung,spleen and heart in different time were collected and the expression of rIL-10 was detected by the methods of RT-PCR,ELISA and immunochemistry.Results Using rIL-10 gene as a reporter gene,the results demonstrated that an efficient transfer and expression of rIL-10 in rat liver could be achieved by a rapid injection of a large volume of rIL-10 DNA solution into rat via tail vein.Maintaining a stable expression of rIL-10 in serum could be assessed by repeated administration.Conclusion The HBT was a simple,convenient and efficient method of gene transfer and expression in rats,which could be used as an effective means to study further gene therapy of rIL-10 in liver diseases.