ABSTRACT
Objective To study the influence of penehyclidine hydrochloride(PHC)on inflammatory factors in patients with acute lung injury(ALI).Methods Total of 96 patients with ALI were randomly divided into treatment group(48 cases)and control group(48 cases).Patients in the treatment group were given conventional therapy,plus penehyclidine hydrochloride injection 1 mg,im,q12 h or q8h,the first dose could be doubled,at least 2 days of continuous application;Patients in the control group were received conventional therapy.Tumor necrosis factor α (TNF-α),interleukin-6 (IL-6),high sensitive C reactive protein (hs-CRP),calcitonin (PCT),oxygenation index (PaO2/FiO2),lung injury score (LIS) and acute physiology and chronic health status score (APACHE II) of patients on each time point were compared between the two groups before and after treatment,and mechanical ventilation time,intensive care (ICU) treatment time,acute respiratory distress syndrome (ARDS) and ICU mortality were recorded.Results On each time point of treatment,TNF-α,IL-6,hs-CRP,PCT,LIS,APACHE II in treatment group were significantly lower than that of control group (P<0.05),PaO2/FiO2 was significantly higher than that of control group(P<0.01).The mechanical ventilation time,ICU treatment time in treatment group were shorter than that of control group(all P<0.05),The incidence of ARDS in treatment group and control group was 20.8% and 39.6%,respectively(P<0.05);ICU mortality rate was 12.5% and 31.2%,respectively(P<0.05).Conclusion Penehyclidine hydrochloride can effectively improve the oxygen metabolism in acute lung injury,regulate the pulmonary inflammatory response and improve the prognosis of patients.
ABSTRACT
Objective To explore the inhibitory effect and possible mechanisms of lianhuaqingwen capsules on radiation-induced acute lung injury in rats. Methods Rats were randomly divided into control group, radiation group and radiation plus lianhuaqingwen group, the control group and the radiation group rats were given 0. 9% sodium chloride solution, the radiation plus lianhuaqingwen group rats were given lianhuaqingwen 0. 9% chlorine sodium solution. HE staining was applied to test the lung tissue inflammation; quantitative RT-PCR and ELISA were used to measure the content of IL-6, TNF-α and MCP-1 in rats;immunohistochemical assay was taken to detect the infiltration of macrophage in lung tissues. Results The relative mRNA expression of IL-6, TNF-α and MCP-1 in the control, radiation model control and radiation plus Lianhuaqingwen groups were (0. 002 1±0. 000 20),(0. 006 6±0. 000 32),(0. 003 9±0. 000 22); (0. 003 7±0. 000 16),(0. 007 4±0. 000 33),(0. 005 5± 0.000 24);(0.001 4±0.000 15),(0.005 4±0.000 72),(0.003 2±0.000 17),respectively; the concentration (pg·mL-1) of IL-6,TNF-αand MCP-1 in the serum were (35. 2±10. 9),(111. 8±26. 1),(68. 2±15. 2); (229. 3±28. 5),(837. 5±57. 6), (566. 9±39. 8);(96. 85±8. 20),(314. 53±12. 76),(191. 32±10. 97),respectively; and the macrophages at high magnification field in each group were (59. 5±4. 3),(503. 9±25. 8)and (106. 2±12. 6), respectively. Lianhuaqingwen capsules significantly alleviated the lung inflammation in rats with radiation-induced acute lung injury,inhibited the accumulation of macrophage in lung tissue,reduced the expression of IL-6 and TNF-α,and decreased the content of MCP-1 in lung tissues and sera(P<0. 05). Conclusion Lianhuaqingwen capsules attenuated the lung inflammation developed in rats with radiation-induced acute lung injury through inhibiting the expression of MCP-1 and reducing the accumulation of macrophage in lung tissues.
ABSTRACT
Objective To investigate the protection mechanism of ulinastatin on bacterial endotoxin-induced acute lung injury. Methods Acute lung injury was induced by Escherichia colilipo-polysaccharide(LPS)5 mg·kg-1·d-1,intratracheally. Twenty SD rats were randomly divided into control group(n=10)and ulinastatin group(n=10). Ulinastatid group received ulinastatin 50 kU·kg-1 ,the control groups received the same amount of 0. 9% sodium chloride solution. Then the expression changes of rat AQP-1 and AQP-5,alveolar wall thickness change and the degree of pulmonary edema were detected. Results After the injection of LPS into the rat,the expression of AQP-1 and AQP-5 in control group were continuously decreased,but those in ulinastatin group decreased were not obvious. The lung wet/dry weight ratio in the control group increased significantly,the not obvious changes in the ulinastain group. The thickness of the alveolar in 24,48,72 h of the control group were(3. 84±0. 68),(6. 32±1. 08),(11. 03±2. 47)μm, respectively,and those in the ulinastian groups were(2. 31±0. 44)(,3. 76±0. 82)(,2. 94±0. 67)μm,respectively. Conclusion The AQP-1 and AQP-5 induced the occurrence of pulmonary edema by changing the cell permeability. Ulinastatin can slow down the process so as to reduce the degree of endotoxin-induced lung injury.
