摘要
Objective： To investigate the role of Shenfu Injection （参附注射液, SFI） in rats with systemic inflammatory response syndrome （SIRS）. Methods： The SIRS rat model was induced by the intravenous injection of lipopolysaccharide （LPS）. Forty-five male Wistar rats were randomly divided into 3 groups, the sham operative control group （control group, n=5）, the SIRS model group （model group, n=20） and the SFI treatment group （SFI group, n=20）. LPS was injected through the external jugular vein （12 mg/kg, 6 mg/mL） to all rats except for those in the control group, and SFI （10 mL/kg） was given to those in the SF group only once through intraperitoneal injection, while the normal saline （10 mL/kg） was given to those in the model group. For those in the control group, normal saline was given through the external jugular vein （2 mL/kg） and intraperitoneal injection （10 mL/kg）. Then, rats in the model group and SFI group were divided into 4 subgroups according to the time points, i.e., 1 h, 2 h, 4 h and 6 h subgroups, 5 rats in each group. The activity of nuclear factor of κB （NF-κB） of in blood mononuclear cells and the plasma levels of tumor necrosis factor- α （TNF- α ） and interleukin 6-（IL-6） were determined using enzyme-linked immunoabsordent assay （ELISA） at 1 h, 2 h, 4 h and 6 h after modeling. Histopathologic changes of the lung and liver were observed under a light microscope. Results： Compared with the control group, the activity of NF-κB in mononuclear cells and the plasma level of TNF-α were obviously increased at each time points （all P〈0.01）, reaching the peaks at 2 h after modeling. The plasma level of IL-6 increased gradually as time went by in the model group （P〈0.01）. Pathological examination showed pulmonary alveoli hemorrhage, edema and inflammatory cell infiltration in the lung tissue, and angiotelectasis, congestion, and local necrosis in the liver tissue in the model group. Compared with the model group, the activity of NF- κB and the levels of TNF-α and IL-6 in plasma decreased significantly in the SFI group （P〈0.01）, and the pathological injury in the lungs and liver was significantly alleviated. Conclusion： SFI plays a protective role by inhibiting the activity of NF-κB, and reducing the expressions of TNF-α and IL-6 in SIRS rats.
Objective： To investigate the role of Shenfu Injection （参附注射液, SFI） in rats with systemic inflammatory response syndrome （SIRS）. Methods： The SIRS rat model was induced by the intravenous injection of lipopolysaccharide （LPS）. Forty-five male Wistar rats were randomly divided into 3 groups, the sham operative control group （control group, n=5）, the SIRS model group （model group, n=20） and the SFI treatment group （SFI group, n=20）. LPS was injected through the external jugular vein （12 mg/kg, 6 mg/mL） to all rats except for those in the control group, and SFI （10 mL/kg） was given to those in the SF group only once through intraperitoneal injection, while the normal saline （10 mL/kg） was given to those in the model group. For those in the control group, normal saline was given through the external jugular vein （2 mL/kg） and intraperitoneal injection （10 mL/kg）. Then, rats in the model group and SFI group were divided into 4 subgroups according to the time points, i.e., 1 h, 2 h, 4 h and 6 h subgroups, 5 rats in each group. The activity of nuclear factor of κB （NF-κB） of in blood mononuclear cells and the plasma levels of tumor necrosis factor- α （TNF- α ） and interleukin 6-（IL-6） were determined using enzyme-linked immunoabsordent assay （ELISA） at 1 h, 2 h, 4 h and 6 h after modeling. Histopathologic changes of the lung and liver were observed under a light microscope. Results： Compared with the control group, the activity of NF-κB in mononuclear cells and the plasma level of TNF-α were obviously increased at each time points （all P〈0.01）, reaching the peaks at 2 h after modeling. The plasma level of IL-6 increased gradually as time went by in the model group （P〈0.01）. Pathological examination showed pulmonary alveoli hemorrhage, edema and inflammatory cell infiltration in the lung tissue, and angiotelectasis, congestion, and local necrosis in the liver tissue in the model group. Compared with the model group, the activity of NF- κB and the levels of TNF-α and IL-6 in plasma decreased significantly in the SFI group （P〈0.01）, and the pathological injury in the lungs and liver was significantly alleviated. Conclusion： SFI plays a protective role by inhibiting the activity of NF-κB, and reducing the expressions of TNF-α and IL-6 in SIRS rats.
基金
Supported by a Grant from Hubei Province Science and Technique Foundation(No.2003AA301C51)
