Objective　To study the effect of IFN-γ inhalation via aerosol on cytokines of the immunocompromised rats. Methods　Immunocomprised rat model was established with cortisol acetate injection for 14 d and then Candida albicans fluid was injected by tracheal for establishing am immuno comprised with pulmonary infection model. IFN-γ was inhaled with aerosol 1 d before the bacterium injection and then for 1, 3 and 7 d respectively. The activity of TNF-α, and the levels of IL-1β and IL-6 in the supernatant of the cultured alveolar macrophage(AM), the activity of IFN-γ and TNF-α in bronchial alveolar lavage fluid (BALF), the expressions of IFN-γ,TNF-α, IL-1β, and IL-6 of the lung tissues, the level of IFN-γ,IL-1β, and IL-6 in the serum were investigated. Results　The activity of TNF-α, and the levels of IL-1β and IL-6 in the culture supernatant of the AM of the rats treated with IFN-γ were significantly higher than those of the control. The activity of IFN-γ and TNF-α in BALF was higher in the IFN-γ inhaled rats than in the control (except the activity of TNF-α on the 7th day). The expressions of IFN-γ and IL-1β in lung tissues was higher in the rats treated with IFN-γ than in the control. The expression of TNF-α in the rats treated with IFN-γ was less than that in the control rats. The expression of IL-6 had no difference between 2 groups. And no difference was found in the activity of IFN-γ, and the levels of IL-1β and IL-6 in the serum between 2 groups(except IL-1β on the 3rd day). Conclusion　Administration of IFN-γ via aerosol can obviously increase the activity or levels of some cytokines in the lung of the immunocompromised rats, but has no effect on them in serum of the immunocompromised rats.

The article presents the experience, reformation and research of clinical teaching program in the indirectly affiliated school of clinical medicine. The exploration for the establishment of a new teaching mechanism in the school of clinical medicine is implemented.

Mitochondrial dysfunction is closely related to the occurrence and development of benign and malignant diseases of the pancreas. Mitochondrial membrane of the respiratory chain electron transfer and energy transfer plays an important role in maintaining normal cellular function. When the respiratory chain was disrupted, the oxidative stress was increased in the cell, and produced a large number of oxide intermediate products which target mitochondrial protein, DNA, etc, lead to mitochondrial dysfunction finally induced acute pancreatitis, pancreatic cancer and other diseases. In addition, mitochondrial homeostasis plays an indispensable role in maintaining the normal function of islet cells. This paper reviewed the research status of mitochondrial dysfunction in pancreatic diseases.

ObjectiveTo investigate the protective effect of tanshinone I (T-I) on hepatic ischemia-reperfusion injury (HIRI) in mice. MethodsA total of 36 C57BL/6J mice were randomly divided into sham-operation group, ischemia-reperfusion (IR) group, IR+T-I (5 mg/kg) group, IR+T-I (10 mg/kg) group, IR+T-I (20 mg/kg) group, and IR+T-I (40 mg/kg) group, with 6 mice in each group. Each group was given intraperitoneal injection. The mice in the sham-operation group and the IR group were injected with an equal volume of the solvent olive oil; the mice in the IR+T-I groups were administered once a day for 7 consecutive days, a model of 70% HIRI was established at 2 hours after the last administration, and serum and liver samples were collected after 6 hours of reperfusion. Related kits were used to measure the serum level of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and the content of superoxide dismutase (SOD), malondialdehyde (MDA), caspase-3, and reduced glutathione (GSH) in liver tissue; HE staining was used to observe liver histopathology; the TUNEL method was used to measure the level of hepatocyte apoptosis; immunohistochemistry was used to measure the protein expression of caspase-3 and heme oxygenase-1 (HO-1). A one-way analysis of variance was used for comparison of continuous data between multiple groups, and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the IR group, the IR+T-I (20mg/kg) group had significant reductions in the serum levels of ALT (192.48±23.67 U/L vs 336.90±41.52 U/L, P＜0.01) and AST (123.19±9.16 U/L vs 206.90±18.81 U/L, P＜0.01), and thus 20 mg/kg was determined as the optimal concentration. Compared with the IR group, the IR+T-I (20 mg/kg) group had significant reductions in MDA (1.34±0.21 μmol/mg vs 3.48±0.95 μmol/mg, P＜0.05) and caspase-3 (0.69±0.97 μmol/mg vs 1.04±0.35 μmol/mg, P＜0.05) and significant increases in SOD (274.47±30.53 U/mg vs 160.29±27.37 U/mg, P＜0.05) and GSH (2.12±0.27 μmol/mg vs 1.03±0.42 μmol/mg, P＜0.05). HE staining showed that the IR group had disordered structure of hepatic lobules and focal or extensive degeneration and necrosis of hepatocytes; compared with the IR group, the IR+T-I (20 mg/kg) group had a reduction in the area of hepatocyte necrosis and a basically complete structure of the liver. Immunohistochemistry showed that compared with the IR group, the IR+T-I (20 mg/kg) group had significant reductions in the number of apoptotic hepatocytes and the protein expression of caspase-3 and a significant increase in the protein expression of HO-1. ConclusionT-I exerts a protective effect against HIRI in mice by inhibiting liver oxidative stress response and hepatocyte apoptosis.