Expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cell of chronic arsenic poisoning rats
10.3760/cma.j.issn.1000-4955.2012.05.015
- VernacularTitle:半胱氨酸蛋白酶-8和P53在慢性砷中毒大鼠肾近端小管表达的研究
- Author:
Li-quan, QIAN
;
Yuan-hui, LI
;
Xiang-zhao, KONG
;
Ting-ting, JIN
;
Na, LI
- Publication Type:Journal Article
- Keywords:
Arsenic poisoning;
Rats;
Renal proximal tubular;
Cysteine caspase-8;
P53
- From:Chinese Journal of Endemiology
2012;31(5):531-533
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the molecular mechanism of renal injury of chronic arsenic poisoning rats induced by the expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells.Methods Sixty healthy SD rats were divided into three groups,high-,low-dose group,and control group,n =20 in each group.The rats in high and low dose groups were treated with As203 through drinking water,10.0 and 0.4 mg/kg,respectively.The control rats were given distilled water.Four months later,serum and urinary arsenic level was determined,and kidney specimens were taken.The expression of cysteine caspase-8 and P53 in renal proximal tubular epithelial cells was detected by histological technique-HE staining and SABC immunohistochemistry.In addition,cell number counting and image analyses were used in the study.Results The number of caspase-8 positive cells of renal proximal tubule in control group,low-and high-dose group was 3.33±1.32,31.14±8.02 and 46.50±7.20 cell number/visual fields,respectively,which was increased with dose increasing(all P ＜0.05);the average gray value was 151.34±6.40,133.58±4.63 and 128.34±16.28,respectively,decreased with dose increasing(all P ＜0.05).The number of P53 positive cells was 3.17±1.59,26.29±4.23 and 47.00±6.22 cell number/visual fields,respectively,increased with dose increasing (all P ＜ 0.05) ; the average gray value was 142.54±8.06,121.48±5.68 and 101.89±6.35,respectively,decreased with dose increasing (all P ＜ 0.05).Conclusion The increase of caspase-8 and P53 positive cells is one of the molecular mechanisms of renal injury induced by arsenic poisoning.
