中华劳动卫生职业病杂志
中華勞動衛生職業病雜誌
중화노동위생직업병잡지
CHINESE JOURNAL OF INDUSTRIAL HYGIENE AND OCCUPATIONAL DISEASES
2014年
5期
335-339
,共5页
查晚生%冷静%王峰%张家祥%李树龙%王慧%沈彤%朱启星
查晚生%冷靜%王峰%張傢祥%李樹龍%王慧%瀋彤%硃啟星
사만생%랭정%왕봉%장가상%리수룡%왕혜%침동%주계성
三氯乙烯%小鼠%补体
三氯乙烯%小鼠%補體
삼록을희%소서%보체
Trichloroethylene%Mice%Complement
目的 检测三氯乙烯(TCE)致敏小鼠不同时期肾脏中补体C3a和C5a水平,探讨在TCE致敏引起的肾损伤中补体的作用.方法 小鼠经皮内注射和腹部涂抹TCE 2次致敏后激发.在末次激发后的24 h、48 h、72 h和7d4个时间点采血、取肾脏,用全自动生化分析仪检测血清中尿索氮(BUN)和肌酐(Cr)水平,免疫组织化学法检测肾脏中C3a和C5a沉积水平.结果 TCE处理组的小鼠致敏率达到42.0％.与溶剂对照组比较,致敏48 h和72 h组小鼠肾脏系数、血清BUN和Cr水平均明显升高,差异有统计学意义(P＜0.05).与同时点末致敏组比较,48 h和72 h致敏组小鼠肾脏系数明显增大,差异有统计学意义(P＜0.05).与溶剂对照组比较,7d致敏组肾脏系数、血清BUN、Cr水平差异无统计学意义(P＞0.05).与溶剂对照组比较,致敏48 h组小鼠肾脏补体C3a(3.80±0.84)、C5a (4.00± 1.00)水平明显升高,差异有统计学意义(P＜0.05);致敏72 h组小鼠肾脏中补体C3a(4.40±1.14)、C5a(4.40±1.14)水平明显高于溶剂对照组,差异有统计学意义(P＜0.05).7d致敏组小鼠肾脏中补体C3a(1.80±0.45)、C5a (2.00±0.71)水平与溶剂对照组比较,差异无统计学意义(P＞0.05).结论 TCE致敏可引起小鼠肾功能损伤,补体C3a和C5a在致敏小鼠肾脏中的水平升高,提示补体C3a和C5a可能参与TCE致敏引起的肾脏损伤.
目的 檢測三氯乙烯(TCE)緻敏小鼠不同時期腎髒中補體C3a和C5a水平,探討在TCE緻敏引起的腎損傷中補體的作用.方法 小鼠經皮內註射和腹部塗抹TCE 2次緻敏後激髮.在末次激髮後的24 h、48 h、72 h和7d4箇時間點採血、取腎髒,用全自動生化分析儀檢測血清中尿索氮(BUN)和肌酐(Cr)水平,免疫組織化學法檢測腎髒中C3a和C5a沉積水平.結果 TCE處理組的小鼠緻敏率達到42.0％.與溶劑對照組比較,緻敏48 h和72 h組小鼠腎髒繫數、血清BUN和Cr水平均明顯升高,差異有統計學意義(P＜0.05).與同時點末緻敏組比較,48 h和72 h緻敏組小鼠腎髒繫數明顯增大,差異有統計學意義(P＜0.05).與溶劑對照組比較,7d緻敏組腎髒繫數、血清BUN、Cr水平差異無統計學意義(P＞0.05).與溶劑對照組比較,緻敏48 h組小鼠腎髒補體C3a(3.80±0.84)、C5a (4.00± 1.00)水平明顯升高,差異有統計學意義(P＜0.05);緻敏72 h組小鼠腎髒中補體C3a(4.40±1.14)、C5a(4.40±1.14)水平明顯高于溶劑對照組,差異有統計學意義(P＜0.05).7d緻敏組小鼠腎髒中補體C3a(1.80±0.45)、C5a (2.00±0.71)水平與溶劑對照組比較,差異無統計學意義(P＞0.05).結論 TCE緻敏可引起小鼠腎功能損傷,補體C3a和C5a在緻敏小鼠腎髒中的水平升高,提示補體C3a和C5a可能參與TCE緻敏引起的腎髒損傷.
목적 검측삼록을희(TCE)치민소서불동시기신장중보체C3a화C5a수평,탐토재TCE치민인기적신손상중보체적작용.방법 소서경피내주사화복부도말TCE 2차치민후격발.재말차격발후적24 h、48 h、72 h화7d4개시간점채혈、취신장,용전자동생화분석의검측혈청중뇨색담(BUN)화기항(Cr)수평,면역조직화학법검측신장중C3a화C5a침적수평.결과 TCE처리조적소서치민솔체도42.0％.여용제대조조비교,치민48 h화72 h조소서신장계수、혈청BUN화Cr수평균명현승고,차이유통계학의의(P＜0.05).여동시점말치민조비교,48 h화72 h치민조소서신장계수명현증대,차이유통계학의의(P＜0.05).여용제대조조비교,7d치민조신장계수、혈청BUN、Cr수평차이무통계학의의(P＞0.05).여용제대조조비교,치민48 h조소서신장보체C3a(3.80±0.84)、C5a (4.00± 1.00)수평명현승고,차이유통계학의의(P＜0.05);치민72 h조소서신장중보체C3a(4.40±1.14)、C5a(4.40±1.14)수평명현고우용제대조조,차이유통계학의의(P＜0.05).7d치민조소서신장중보체C3a(1.80±0.45)、C5a (2.00±0.71)수평여용제대조조비교,차이무통계학의의(P＞0.05).결론 TCE치민가인기소서신공능손상,보체C3a화C5a재치민소서신장중적수평승고,제시보체C3a화C5a가능삼여TCE치민인기적신장손상.
Objective To determine the levels of complement components C3a and C5a in the kidneys of trichloroethylene (TCE)-sensitized BALB/c mice,and to investigate the role of complement components in TCE-induced renal injury among BALB/c mice.Methods Sixty-two female BALB/c mice were randomly divided into blank control group,vehicle control group,and TCE sensitization group.The mice in TCE sensitization group were sensitized by one intracutaneous injection and one abdominal smear of TCE.At 24 h,48 h,72 h,and 7 d after the second sensitization,mice were sacrificed,and the blood and kidneys were collected.An automatic biochemical analyzer was used in the determination of serum blood urea nitrogen (BUN) and creatinine (Cr).The levels of C3a and C5a in the kidneys were determined by immunohistochemistry.Results The sensitization rate of TCE sensitization group was 42.0％.Kidney coefficient and serum levels of BUN and Cr were significantly increased in the TCE sensitization group as compared with the vehicle control group at 48 h and 72 h after sensitization (P＜0.05).The kidney coefficients of the TCE sensitization group at 48 h and 72 h were significantly higher than those of the control groups (P＜0.05).In comparison with the vehicle control group,however,no significant change was found in kidney coefficient,serum BUN,or serum Cr at 7 d after TCE sensitization (P＞0.05).Levels of C3a and C5a at 48 h (3.80±0.84 and 4.00±1.00,respectively) and 72 h (4.40±1.14 and 4.40±1.14,respectively) after sensitization were all significantly higher than those of the vehicle control group (P＜0.05),but no significant difference was found in level ofC3a (1.80±0.45) or C5a (2.00± 0.71) at 7 d (P＞0.05).Conclusion TCE sensitization can induce renal injury in mice.Levels of complement components C3a and C5a are elevated in the kidneys of sensitized mice,indicating that C3a and C5a may be involved in the renal injury induced by TCE sensitization.
