Morphological changes of rat cardiac tissue caused by citreoviridin combined with selenium and protein deficiency / 中国地方病学杂志

ABSTRACT

ObjectiveTo observe the morphological feature of myocardial changes in adult rat exposed to citreoviridin(CIT) with selenium and protein deficiency.MethodsAccording to 2 × 2 factorial design,48 healthy male Wistar rats aged 4-week were randomly divided into four groupsgroup Ⅰ (Se-Pro-CIT+,low selenium and low protein plus CIT group),group Ⅱ (Se-Pro-CIT-,low selenium and low protein without CIT group),group Ⅲ (Se+Pro+CIT+,adequate selenium and adequate protein plus CIT group),and group Ⅳ (Se+Pro+CIT-,adequate selenium and adequate protein without CIT group),12 rats in each group.After one week of normal adaptive feeding,all the rats were fed with selenium and protein deficiency feed for 2 months,and then the animals in group Ⅰ and group Ⅲwere fed with 8 mg·kg-1 ·d-1 of CIT for 2 more months,after that the CIT dose was increased to 10 mg·kg-1 ·d-1 for the final 2 weeks.At the end of the experiment,all the rats were sacrificed by femoral artery bleeding,and body and heart weight were measured.Heart weight index was calculated and histopathological changes were observed under light microscope.Results Heart weight indexes of the 4 groups(Se-Pro-CIT+,Se-Pro-CIT-,Se+Pro+CIT+ and Se+Pro+CIT- groups) were (3.65 ± 0.45) × 10-3,(3.05 ± 0.19) × 10-3,(3.83 ± 1.06) × 10-3 and (3.31 ± 0.52) × 10-3,respectively.The results of factorial analysis showed that the effects of CIT on heart weight index were statistically significant(F =8.524,P ＜ 0.05 ),the effects of Se + Pro were not statistically significant(F =1.347,P ＞ 0.05),and there were no interactions between the two factors (F =0,048,P ＞ 0.05).Morphologically,tissue fibrosis around branch coronary artery in group Ⅰ rats,plenty of cardiocyte pycnosis in group Ⅱ,and myocardial scattered necrotic foci in group Ⅲ were observed,accompanied by inflammatory cell infiltration in group Ⅲ,and normal myocardial structure in group Ⅳ rats.Conclusions Citreoviridin plays a major role in causing myocardial injury( degeneration and necrosis) and CIT combined with selenium and protein deficiency can aggravate the