| Objective To discuss the oxidative damage effect of PM2.5in cooking oil fume onalveolar type Ⅱ epithelial cells of fetal rat （AECⅡ）, and the protective effect of NACrelated to the oxidative damage PM2.5has done to alveolar type Ⅱepithelial cells offetal rat （AEC Ⅱ）, in order to provide experimental evidence for the mechanism ofoxidative damage of cooking oil fume PM2.5on lungs.Method Use PM2.5sampler to collect some fine particles as toxic substances, and useDMSO to prepare liquid with apoptotic cells. Extract some lung tissue of embryonicrat in female rats with18days pregnancy, and extract some alveolar type Ⅱepithelialcells from these lung tissue of fetal rat as the experimental target cells. The MTTmethod can determine the relation between the concentration of cooking oil fumePM2.5and the survival rate of AECⅡ. The kit of MDA,SOD and GSH can detect theoxidative damage effect of particles on cells and the anti-oxidative stress effect ofNAC.Results1.Different density particulates act on AECⅡ36hseparately, they produce obviouscytotoxicity and has a relationship between dose and reflection, the cell viability arisesafter NAC interference.2.Comparing to control group, AECⅡ SOD viability of25μg/ml group,50μg/mlgroup,75μg/ml group decline after36h contamination, the differences has the statistics significance （P<0.05）. Comparing to12.5μg/ml group, the AEC ⅡSOD viability of the20μg/ml group,50μg/ml group,75μg/ml group all decline, the differences has thestatistics significance （P<0.05）. Comparing to25μg/ml group, the AEC ⅡSODviability of the75μg/ml group and NAC interference group, all decline, the differenceshas the statistics significance （P<0.05）. Comparing to control group, the AEC ⅡMDAof12.5μg/ml,50μg/ml,75μg/ml all increase, the differences has the statisticssignificance （P<0.05）. Comparing to25μg/ml group, the AEC ⅡMDA of the75μg/mlgroup increase, the differences has the statistics significance （P<0.05）. Comparing to75μg/ml group, the AEC Ⅱ MDA of the NAC interference groupdecline, thedifferences has the statistics significance （P<0.05）. Comparing to control group,AEC ⅡGSH of50μg/ml group,75μg/ml group both decline, the differences has thestatistics significance （P<0.05）. The comparing of each density AEC ⅡGSH in PM2.5contamination fetal rats has no statistics significance after different contaminationtime.Conclusion Cooking oil fume PM2.5has produced some cytotoxicity and oxidativedamage on AECⅡ of fetal rat, and the antioxidant NAC can resist the oxidativedamage effect of PM2.5on AECⅡ of fetal rat. Objective To discuss the effect of PM2.5in cooking oil fume on the change of proteinamount of alveolar epithelial cells （AEC Ⅱ） endoplasmic reticulum molecularchaperon glucose-regulated protein78（Glucose-Regulated Protein78, Grp78） andendoplasmic reticulum apoptosis caspase-12, and the antagonism of NAC on cellapoptosis, to provide further theoretical and experimental basis for acknowledgmentand understanding of toxicological mechanism of cooking oil fume PM2.5on lungs.Method Use PM2.5sampler to collect some fine particles as toxic substances, dilutedinto apoptotic cell liquid with different concentration. Extract some alveolartypeⅡ epithelial cells from lung tissue of18-day ICR fetal rat as the experimentaltarget cells. Western Blot determines the reticulum pathway of cooking oil fume PM2.5on apoptosis of AEC Ⅱ in endoplasmic and the relatedexpressions of protein GRP-78,Caspase-12.Results The result of Western-blot shows that unfolded protein response （UPR）chaperonin GRP78, Caspase12are dynamic after contamination for36h.1.GRP78protein bands expression, comparing to control group,12.5μg/ml,50μg/ml,75μg/ml and75μg/ml+10mmol/LNACPM2.5contamination group protein expression quantityincreases, the difference has the statistical significance （P<0.05）; comparing to12.5μg/ml group,25μg/ml,50μg/ml,75μg/ml and75μg/ml+10mmol/LNACPM2.5contamination group protein expression quantity increases, the difference has thestatistical significance （P<0.05）; comparing to25μg/ml group,50μg/ml and 75μg/ml+10mmol/LNACPM2.5contamination group protein expression quantityincreases，75μg/ml protein expression decreased, the difference has the statisticalsignificance （P<0.05）; comparing to50μg/ml group,75μg/ml and75μg/ml+10mmol/LNAC protein expression decreased， the difference has thestatistical significance （P<0.05）; comparing to75μg/ml group,75μg/ml+10mmol/LNAC protein expression increases, the difference has the statisticalsignificance （P<0.05）.2.Caspase-12banding protein expression, comparing to controlgroup,25μg/ml,50μg/ml,75μg/ml and75μg/ml+10mmol/LNACPM2.5contaminationgroup protein expression quantity increases, the difference has the statisticalsignificance （P<0.05）; comparing to12.5μg/ml group,25μg/ml,50μg/ml,75μg/ml and75μg/ml+10mmol/LNACPM2.5contamination group protein expression increases, thedifference has the statistical significance （P<0.05）; comparing to25μg/ml group,50μg/ml,75μg/ml and75μg/ml+10mmol/LNACPM2.5contamination group proteinexpression increases, the difference has the statistical significance （P<0.05）;comparing to50μg/ml group,75μg/ml protein expression decreased,75μg/ml+10mmol/LNAC protein expression increases, the difference has the statisticalsignificance （P<0.05）; comparing to75μg/ml group, the protein expression of75μg/ml+10mmol/LNAC interference group increases, the difference has the statisticalsignificance （P<0.05）.Conclusion Cooking oil fume PM2.5induces the apoptosis of AECⅡ by theendoplasmic reticulum, and NAC cells has a protective effect on the apoptosis. |
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