Abstract:Objective To investigate the effect of curcumin on oxidative stress in lung induced by thoracic blast exposure and its possible molecular mechanism.Methods Thirty C57BL/6 mice were randomly divided into control group,model group and model with curcumin group.Collect lung tissue at 24 h after thoracic blast exposure.The left lung was fixed in 10% formalin and embedded in paraffin.The right lung was preserved at -80 ℃.Hematoxylin-eosin staining was used to detect the pathological changes of lung tissue,and ROS was used to detect the oxidative stress injury.Western blot was used to detect the expression of MDA5,SOD-1,IRE-α,p-PI3K,Nrf2 and Keap1.Results After chest blast,the cell arrangement of lung tissue in model group was obviously disordered,cell degeneration and inflammatory cell infiltration were observed.Compared with the control group,the blue fluorescence decreased and the red fluorescence increased significantly in the model group under UV excitation.Western blot showed that the relative density of MDA5,IRE-α,SOD-1,Nrf2 and Keap1 in the model group were 0.68±0.08,0.63±0.04,0.38±0.02,0.32±0.03 and 0.98±0.11,respectively.These proteins in the control group were 0.33±0.03,0.29±0.02,0.81±0.09,0.43±0.05 and 0.44±0.04,respectively.The relative density of p- PI3K/PI3K in the model group was 0.74±0.05,which was significantly higher than that of the control group (0.30±0.02).The differences above were statistically significant (P<0.05).After curcumin intervention,comparing with the model group,HE staining showed that the degeneration and necrosis of lung tissue and the infiltration of inflammatory cells were alleviated.ROS detection showed that the blue fluorescence increased and the red fluorescence decreased significantly in the model with curcumin group.Western blot showed that the relative density of MDA5,IRE-α,SOD-1,Nrf2 and Keap1 in model with curcumin group were 0.48±0.07,0.36±0.06,0.51±0.07,0.71±0.08 and 0.53±0.06,respectively,and the relative density of p-PI3K/PI3K was 0.56±0.07.The above differences were statistically significant compared with the model group (P<0.05).Conclusions Curcumin can protect lung tissue from oxidative stress injury induced by thoracic blast exposure,and the mechanism may be associated with PI3K/Nrf2/Keap1 signaling pathway.
Shaikh S B,Bhat S G,Bhandary Y P.Curcumin attenuates il-17a mediated pulmonary smad dependent and non-dependent mechanism during acute lung injury in vivo[J].Mol Biol Rep,2020,47(7):5643-5649.
[6]
Tang F,Ling C.Curcumin ameliorates chronic obstructive pulmonary disease by modulating autophagy and endoplasmic reticulum stress through regulation of sirt1 in a rat model[J].J Int Med Res,2019,47(10):4764-4774.
[7]
Liu Y,Tong C,Xu Y,et al.Cd28 deficiency ameliorates blast exposure-induced lung inflammation,oxidative stress,apoptosis,and t cell accumulation in the lungs via the pi3k/akt/foxo1 signaling pathway[J].Oxid Med Cell Longev,2019,2019:4848560.
[8]
Rodriguez L R,Bui S N,Beuschel R T,et al.Curcumin induced oxidative stress attenuation by n-acetylcysteine co-treatment:A fibroblast and epithelial cell in-vitro study in idiopathic pulmonary fibrosis[J].Mol Med,2019,25(1):27.
[9]
Cong P,Liu Y,Liu N,et al.Cold exposure induced oxidative stress and apoptosis in the myocardium by inhibiting the nrf2-keap1 signaling pathway[J].BMC Cardiovasc Disord,2018,18(1):36.
[10]
Wang Y,Wang X,Zhang L,et al.Alleviation of acute lung injury in rats with sepsis by resveratrol via the phosphatidylinositol 3-kinase/nuclear factor-erythroid 2 related factor 2/heme oxygenase-1 (pi3k/nrf2/ho-1) pathway[J].Med Sci Monit,2018,24:3604-3611.
[11]
Chuang C H,Yang C K,Wu P H,et al.Acute renal injury induced by endotoxic shock in rats is alleviated via pi3k/nrf2 pathway[J].Eur Rev Med Pharmacol Sci,2018,22(16):5394-5401.
[12]
Li H,Song F,Duan L R,et al.Paeonol and danshensu combination attenuates apoptosis in myocardial infarcted rats by inhibiting oxidative stress:roles of nrf2/ho-1 and pi3k/akt pathway[J].Sci Rep,2016,6:23693.
[13]
Lelli D,Sahebkar A,Johnston T P,et al.Curcumin use in pulmonary diseases:state of the art and future perspectives[J].Pharmacol Res,2017,115:133-148.