Objective To study the pathology and possible mechanism of experimental hydrochloric acid（HCl） inhalation-indued pulmonary fibrosis in rats.Methods 120 male SD rats were randomly divided into a nomal control group，a bleomycin group，a high dose HCl group，a middle dose HCl group and a low dose HCl group.The bleomycin group was intratracheally injected with bleomycin once to induce pulmonary fibrosis.The three HCl groups were intratracheally injected with HCl once per week.The control group was given saline by the same way.Six rats of each group were randomly sacrificed on day 7，14，28 and 42 respectively.The histological changes of lung tissue were studied by HE and Masson’s trichrome staining.Hydroxyproline level in lung tissue was measured by digestion method.Protein and mRNA expression of transforming growth factor-β1（TGF-β1） were assayed by immunohistochemistry and RT-PCR respectively.Results Alveolitis in three HCl groups was significantl compared to control group，most severe at the second week，then remained at a high level which was equivalent to or exceeded the level of the bleomysin group after 28 days.Pulmonary fibrosis in three HCl groups was also significantly more severe than that in the control group，but milder than that in the bleomysin group.The high-dose and middle-dose HCl groups were not significantly different from the bleomysin group on day 42.There was no difference between three HCl groups in the earlier period，but the high-dose HCl group has a significantly difference from low-dose group on day 42.The content of hydroxyproline in high-dose and middle-dose HCl groups was also significantly higher than that in the control group.On day 42 hydroxyproline content in high-dose HCl dose rather middle –or low dose group was similiar with the level of bleomysin group.Content of TGF-β1 mRNA in three HCl groups was comparable to the level of bleomysin group on day 28 and exceeded on day 42.The expression of TGF-β1 in three HCl groups was not significantly different from the bleomysin group on day 42.Conclusion Experimental acid aspiration might contribute to pulmonary fibrosis in rats.Acid induced alveolar epithelial cell damage，abnormal proliferation and repair and fibrosis could be involved..
Objective To investigate the changes of interleukin-17 ( IL-17) and the effects of propofol in rats with acute lung injury ( ALI) . Methods ALI model was established by hydrochloric acid ( HCl) inhalation in a dose of 2 mL/kg. 35 adultmale SD rats were randomly divided into seven groups, ie.a control group, a HCl group, and five propofol groups ( T24b , T12b , T0 , T1a , T3a groups, respectively) . The T0 ,T24b and T12b groups were pretreated with intraperitoneal propofol injection 0, 24 and 12 hours respectively before HCl inhalation. The T1a and T3a groups were managed by intraperitoneal propofol injection 1 and 3 hours respectively after HCl inhalation. Immunohistochemistry was used to determine the expression of IL-17 in lung tissue. ELISA was adopted to detect the levels of IL-17 and IL-8 in lung tissue homogenate as well as in bronchoalveolar lavage fluid ( BALF) , meanwhile arterial partial pressure of oxygen ( PaO2 ) and myeloperoxidase ( MPO) were measured. Results Those rats in the HCl group appeared respiratory distress, cyanosis, pulmonary edema, and inflammatory cells infiltration in lung tissues after HCl inhalation.The IL-17 levels in lung tissue homogenate as well as in BALF were higher in the HCl group than those in the control group( all P lt; 0. 01) . IL-17 was mainly expressed in alveolar epithelial cells and mononuclear cells in the ALI rats and its expression level was higher than that in the control group. IL-17 concentration in lung tissue homogenate was both correlated with IL-8 concentration in lung tissue homogenate ( r=0. 98, P =0.003) and with the activity of MPO in lung tissue( r=0. 981, P =0. 003) in the HCl group. Mainwhile, a same significant correlation was found between IL-8 level in lung tissue homogenate and the MPO activity in the HCl group( r =0. 961, P =0. 009) . Propofol attenuated lung injury induced by HCl inhalation, especially in T24b group. The concentrations of IL-17 in lung tissue homogenate and in BALF were lower in T24b group when compared with the HCl group( P = 0. 011, P =0. 003, respectively) . Conclusions The expression of IL-17 increases in ALI rats. Pretreatment with propofol by 24 hours has obvious inhibiting effects on inflammatory reaction. Inhibiting IL-17 expression may be one of the mechanisms through which propofol inhibits the inflammatory reaction of ALI.