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Objective To investigate the role and mechanism of PSGL-1 in development of salt-sensitive hypertension in mice. Methods PSGL-1 knockout(PSGL-1 -/-)and wild type(PSGL-1 +/ +)mice were fed a high salt (6% NaCl)or normal salt(0.4% NaCl)diet for three months. Blood pressure was measured under anesthesia via the carotid artery. The status of tissue inflammation and kidney injury was tested by flow cytometry, immunohistochemistry, and western blotting. Results Compared with mice fed a normal salt diet, PSGL-1 +/ +mice fed a high salt diet for three months showed high blood pressure, increased inflammatory cell infiltration in the aorta and skin, and increased inflammatory cytokine expression(interleukin-6, interleukin-1β, and tumor necrosis factor-α)in the kidney, as well as elevated expression of the kidney injury marker, connective tissue growth factor. In contrast, inflammation and kidney injury were not found in PSGL-1 -/-mice fed a high-salt diet. Conclusions In mice,PSGL-1 via inflammation plays a key role in development of hypertension and kidney injury caused by high salt intake.
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Objective:To investigate the clinical effects of stellate ganglion block(SGB) on the stress ulcer in burn patients and explore the underlying mechanisms.Methods:40 patients with burn injury induced stress ulcer were randomized to two groups:SGB group (n=20) and Control group (n=20).SGB group was treated with conventional symptomatic therapy,SGB group underwent SGB every two days for 1 week on the basis of Control group.And the levels of plasma ET-1 and NO were detected using ELISA before and after therapy.And the clinical efficacy of the two groups was observed after the treatment.Results:Compared with the Control group,the levels of plasma ET-1 and NO were markedly lower in the SGB group (P＜0.05),while the clinical efficacy was higher(P＜0.05).Conclusion:SGB could enhance the clinical efficacy stress ulcer in bum patients,which might be related to the decrease of plasma ET-1 and NO levels.
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Objective To investigate the role and mechanism of platelet in the development of salt-sensitive hypertension.Methods 25 Dahl salt-sensitive rats (Dahl SS) were divided into three groups: low-salt diet (0.12% NaCl, LS), high-salt diet (8%NaCl, HS) and high-salt diet + platelet inhibitor (8%NaCl+busulfan, HS+bus).Blood pressures were measured by tail-cuff method.After six weeks, animals were sacrificed.Platelet p-selectin expression, platelet cytosolic Ca2+ concentration, platelet-leukocyte aggregation (PLA) in peripheral blood, and immune cells infiltrated on aortic walls were assessed by flow cytometry, and serum IL-6 level was tested by ELISA in vivo.Platelets purified from SD rats were treated with normal salt (0.9%NaCl) and high salt (1.3%NaCl), then the cytosolic Ca2+ concentration and p-selectin expression of platelet were detected.Results We found that Dahl SS rats with high-salt diet, relative to low-salt diet, presented with high blood pressure and increased the ratio of platelet p-selectin expression, Ca2+ concentration.IL-6 level and PLA in peripheral blood, and the number of infiltrated immune cells on aortic walls were also significantly elevated in high-salt diet group.The whole events were ameliorated by the platelet inhibitor busulfan.Cytosolic Ca2+ concentration and p-selectin expression were also increased in purified platelets treated with high salt than those treated with low salt (P < 0.05).Conclusions Our findings suggest that high salt induced platelet activation with increased Ca2+ concentration may play an important role in the development of salt-sensitive hypertension via vascular inflammation.However, the detailed mechanisms of platelet activation and development of high blood pressure via inflammation induced by high salt intake remain to be determined.
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Aim ToinvestigatewhethertheJAK2/STAT3 signaling pathway regulates prohibitin expres-sion to protect cardiomyocytes against hypoxia/reoxy-genation injury in hydrogen sulfide postconditioning. Methods Primaryculturedcardiomyocytesfromneo-natal rats were divided into 6 groups: control group ( Normal) , hypoxia/reoxygenation group ( H/R ) , hy-drogen sulfide postconditioning group ( NP) , hydrogen sulfide with AG490 group ( N + A ) , AG490 group ( AG) , DMSO group ( DMSO) . The survival percent-age of cardiomyocytes and the release of LDH were tested at pre-hypoxia and reoxygenation 2h. After reox-ygenation, cell apoptosis was detected by flow cytome-try. The expression of t-STAT3, p-SATAT3 and PHB were determined with Western blot analysis. Results No obvious changes were observed among the groups before hypoxia (P <0. 05). After reoxygenation 2h, compared with H/R group, NP group significantly im-proved the survival rate of cardiomyocytes ( P <0. 05 ) , inhibited the release of LDH and the myocardi-al apoptosis ( P <0. 05 ) , meanwhile up-regulated the p-STAT3 and PHB expression. However, AG490 abol-ished the cardioprotection offered by hydrogen sulfide postconditioning and the increase in p-STAT3 and PHB expression.Conclusion Hydrogensulfidepostcondi-tioning may protect cardiomyocytes against hypoxia/reoxygenation injury through the JAK2/STAT3 pathway upregulating the expression of prohibitin.