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OBJECTIVE To study the protective effects of Dachengqi decoction （DCQD） on intestinal septic mice， and to explore the possible mechanisms from the Toll-like receptor 4（TLR4）/myeloid differentiation factor 88（MyD88） signaling pathway. METHODS The SPF male C57BL/6J mice were randomly divided into Sham group， Sham+DCQD-H group， model （CLP） group， DCQD-L group， DCQD-H group and Positive group. The model of intestinal sepsis was established by cecal ligation and puncture in CLP group， DCQD-L group， DCQD-H group and Positive group. Three days before the operation and seven days after the operation， DCQD-L group and DCQD-H group were given DCQD intragastrically at 4， 8 g/kg （calculated by crude drug）， respectively. Positive group was given ulinastatin intraperitoneally 2 h before operation and 7 d after the operation （at 50 000 U/kg）. In Sham group and Sham+DCQD-H group， only cecum of mice was exposed without ligation and puncture. Sham+DCQD- H group was given DCQD intragastrically （8 g/kg，calculated by crude drug） 3 days before the operation and 7 days after the operation. Both the Sham group and CLP group were given normal saline 0.2 mL intragstrically and intraperitoneally each day， for 10 consecutive days. After the operation， the severity of sepsis was assessed， and the 7 d survival rate of mice was assessed. One hour after the last medication， the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in serum and ileum of mice were determined； the pathological and morphological changes of mice’s liver， lung， kidney and ileum were observed； mRNA expressions of the TLR4 and MyD88 in ileum were tested. RESULTS Compared with CLP group， sepsis score， the levels of TNF-α and IL-6 in serum and ileum （except for IL-6 in ileum of DCQD-L group）， damage score of the liver， lung， kidney and ileum， mRNA expressions of TLR4 and MyD88 in ileum were all decreased significantly in DCQD-L group and DCQD-H group （P＜0.05 or P＜0.01）， while 7 d survival rate （except for DCQD-L group） was increased significantly （P＜0.05）. The damage to liver tissue in mice was significantly improved， and inflammation infiltration and apoptosis were reduced； lung tissue damage had been alleviated， with varying degrees of improvement in alveolar atrophy， bleeding and edema； the renal tissue damage was improved and weakened dilation of renal tubular lumen was weakened； the damage and edema of ileal tissue were significantly improved. CONCLUSIONS DCQD may exert a protective role on intestinal septic model mice. The mechanism may be related to the inhibition of systemic inflammation， the reduction of multiple organ damage， and down-regulation of TLR4/MyD88 signaling pathway.
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Objective:To investigate the effect of enteral nutritional support in treating COPD patients with respiratory failure and mechanical ventilation.Methods:40 patients were randomly divided into two groups:high-fat and low-carbohydrate enteral nutritional solution group(HL group) and ordinary enteral nutritional solution group(control group).The volume of expired gas(VE),carbon dioxide production(VCO2),partial pressure of carbon dioxide(PaCO2),respiratory quotient(RQ),serum albumin,immunoglobulin,total lymphocyte count(TLC) were detected.Results:VCO2 and PaCO2 were significantly decreased in HL group compared with control group(P
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AIM: To investigate the expression and function of apoptosis-related protein, Fas, FasL, and Bcl-2 in the pathogenesis of autoimmune thyroiditis. METHODS: Immunohistochemical staining was performed on 20 Hashimoto's thyroiditis (HT), 20 Graves' disease (GD), and 20 thyroid follicular adenoma (TFA, as control). RESULTS: All the cases expressed Fas, mainly on the cell surface and cytoplasm. FasL was found in all except 3 of the TFA. Bcl-2 in 15 of HT, 19 of GD, 17 of TFA. In TFA follicular cells expressed moderate Fas and minimal or absent FasL. In HT, follicles adjacent to infiltrating lymphocytes showed a increased levels of Fas and FasL, but infiltrating lymphocytes exhibited weaker staining of Fas and FasL than thyrocytes. In GD, thyrocytes and lymphocytes showed nearly similar Fas with HT, but rather weaker for FasL than HT. Bcl-2 was nearly similar in GD and TFA, but follicular cells in vicinity of lymphocytes and lymphocytes located in germinal centers of HT tissues exhibited significantly weaker. CONCLUSION: The expression of Fas, FasL and Bcl-2 in Hashimoto's thyroiditis and Graves' disease was nearly similar. Strong FasL expression and weak Bcl-2 expression on the follicles in HT may induce apoptosis. These results provide further proof that the functions of Fas and its ligand and Bcl-2 may play an important part in the pathogenesis of autoimmune thyroid diseases. The lymphocytes do not seem to be directly engaged in the process with their own FasL, but they may provide some cytokines that, in turn, up-regulates Fas and/or FasL leading to apoptosis.