Objective:To investigate the protective effect and mechanism of lithium chloride pretreatment on myocardial ischemia-reperfusion injury(I-RI)in rats.Methods:A total of 60 SD rats were randomly divided into control gro...Objective:To investigate the protective effect and mechanism of lithium chloride pretreatment on myocardial ischemia-reperfusion injury(I-RI)in rats.Methods:A total of 60 SD rats were randomly divided into control group,model group,lithium chloride intervention group and L-arginine methyl ester+lithium chloride intervention group with 15 in each.The I-RI model was established in model group,the Utliium chloride intervention group and L-arginine methyl ester+lithium chloride intervention group by method of seaming along left anterior descending coronary artery myocardial,control group was only opened the chest without seaming,STelevation within 2 min was regarded as modeling success.Model group did not adopted any intervention,lithium chloride intervention group was treated with lithium chloride injection15 mg/kg by jugular venipuncture preoperatively,L-arginine methyl ester+lithium chloride intervention group was treated with intraperitoneal injection of 30mg·kg~(-1)·d~(-1)(L—arginine methyl ester 7 d before the test,and intravenous catheter of 15 mg/kg lithium chloride preoperatively.The hydroxybulyric acid dehydrogenase(HBDH),creatine kinase isoenzyme(CK-MB),superoxide dismutase(SOD),malondialdehyde(MDA)level and nitric oxide synthase(NOS)activites were tested.Each large area of myocardial ischemia tissue was extracted for determination of the MDA content,SOD activity in tissue and serum,and morphological changes of myocardial tissue.Results:SOD activity was highest in lithium chloride intervention group,followed by L-arginine methyl ester+lithium chloride intervention group,control group and model group(P<0.05);SOD activity was highest in L-arginine methyl ester+lithium chloride intervention group intervention group,followed by lithium chloride intervention group,control group and model group(P<0.05).MDA content of myocardial tissue was highest in model group,followed by L-arginine methyl ester+lithium chloride intervention group,the lithium chloride intervention group and control group(P<0.05);serum MDA content was highest in L-arginine methyl ester+lithium chloride intervention group,followed by model group,lithium chloride intervention group and control group(P<0.05).Compared with the control group,serum NOS was significantly higher in model group,lithium chloride intervention group and L-arginine methyl ester+lithium chloride intervention group(P<0.05),there was no statistical difference of serum NOS activity between the three groups(P>0.05);HBDH and CK-MB of plasma were highest in model group,followed by L-arginine methyl ester+lithium chloride intervention group,lithium chloride intervention group and control group(P<0.05).A significantly lighter myocardial damage was observed microscopically in lithium chloride intervention group than that in L-arginine methyl ester+lithium chloride intervention group and model group.Conclusions:lithium chloride pretreatment can significandy reduce the myocardial I-RI,maintain structure and function of myocardial cells,improve the antioxidant ability of myocardial tissue,play an effective role on protecting myocardial I-RI.展开更多
The course and severity of periodontitis can be significantly affected by bacterial virulence as well as host immunity dysfunction. Periodontal tissue destruction has been proved to result from cascade of cytokines sy...The course and severity of periodontitis can be significantly affected by bacterial virulence as well as host immunity dysfunction. Periodontal tissue destruction has been proved to result from cascade of cytokines synthesized by reactive cells upon stimulation by pathogenic bacteria and lipopolysaccharides within their cell membranes. The clinical use of genetically programmed cells, producing substances blocking IL-1, based on recombinant IL-1 antagonist, as well as cytokines activating fibroblasts and osteoblasts to regenerate the destroyed periodontal tissue could prove alternative to the conventional treatment. Another cytokine of interest in respect to periodontitis ethiopathogenesis is soluble tumor necrosis factor receptor I (sTNF RI). Observation of soluble TNF receptors as physiologic inhibitors of TNF led to its administration in therapeutic process as well as in therapy selected cases of aggressive periodontitis.展开更多
基金supported by Target Scientific Research of Zhangjiakou Technology Bureau No.12110044D-2
文摘Objective:To investigate the protective effect and mechanism of lithium chloride pretreatment on myocardial ischemia-reperfusion injury(I-RI)in rats.Methods:A total of 60 SD rats were randomly divided into control group,model group,lithium chloride intervention group and L-arginine methyl ester+lithium chloride intervention group with 15 in each.The I-RI model was established in model group,the Utliium chloride intervention group and L-arginine methyl ester+lithium chloride intervention group by method of seaming along left anterior descending coronary artery myocardial,control group was only opened the chest without seaming,STelevation within 2 min was regarded as modeling success.Model group did not adopted any intervention,lithium chloride intervention group was treated with lithium chloride injection15 mg/kg by jugular venipuncture preoperatively,L-arginine methyl ester+lithium chloride intervention group was treated with intraperitoneal injection of 30mg·kg~(-1)·d~(-1)(L—arginine methyl ester 7 d before the test,and intravenous catheter of 15 mg/kg lithium chloride preoperatively.The hydroxybulyric acid dehydrogenase(HBDH),creatine kinase isoenzyme(CK-MB),superoxide dismutase(SOD),malondialdehyde(MDA)level and nitric oxide synthase(NOS)activites were tested.Each large area of myocardial ischemia tissue was extracted for determination of the MDA content,SOD activity in tissue and serum,and morphological changes of myocardial tissue.Results:SOD activity was highest in lithium chloride intervention group,followed by L-arginine methyl ester+lithium chloride intervention group,control group and model group(P<0.05);SOD activity was highest in L-arginine methyl ester+lithium chloride intervention group intervention group,followed by lithium chloride intervention group,control group and model group(P<0.05).MDA content of myocardial tissue was highest in model group,followed by L-arginine methyl ester+lithium chloride intervention group,the lithium chloride intervention group and control group(P<0.05);serum MDA content was highest in L-arginine methyl ester+lithium chloride intervention group,followed by model group,lithium chloride intervention group and control group(P<0.05).Compared with the control group,serum NOS was significantly higher in model group,lithium chloride intervention group and L-arginine methyl ester+lithium chloride intervention group(P<0.05),there was no statistical difference of serum NOS activity between the three groups(P>0.05);HBDH and CK-MB of plasma were highest in model group,followed by L-arginine methyl ester+lithium chloride intervention group,lithium chloride intervention group and control group(P<0.05).A significantly lighter myocardial damage was observed microscopically in lithium chloride intervention group than that in L-arginine methyl ester+lithium chloride intervention group and model group.Conclusions:lithium chloride pretreatment can significandy reduce the myocardial I-RI,maintain structure and function of myocardial cells,improve the antioxidant ability of myocardial tissue,play an effective role on protecting myocardial I-RI.
文摘The course and severity of periodontitis can be significantly affected by bacterial virulence as well as host immunity dysfunction. Periodontal tissue destruction has been proved to result from cascade of cytokines synthesized by reactive cells upon stimulation by pathogenic bacteria and lipopolysaccharides within their cell membranes. The clinical use of genetically programmed cells, producing substances blocking IL-1, based on recombinant IL-1 antagonist, as well as cytokines activating fibroblasts and osteoblasts to regenerate the destroyed periodontal tissue could prove alternative to the conventional treatment. Another cytokine of interest in respect to periodontitis ethiopathogenesis is soluble tumor necrosis factor receptor I (sTNF RI). Observation of soluble TNF receptors as physiologic inhibitors of TNF led to its administration in therapeutic process as well as in therapy selected cases of aggressive periodontitis.