中国地方病学杂志
中國地方病學雜誌
중국지방병학잡지
CHINESE JOURNAL OF ENDEMIOLOGY
2010年
5期
487-492
,共6页
氟%骨保护素%RANK配体%核因子κβ受体活化因子
氟%骨保護素%RANK配體%覈因子κβ受體活化因子
불%골보호소%RANK배체%핵인자κβ수체활화인자
Fluorine%Osteoprotegerin%RANK ligand%Receptor activator of nuclear factor-kappa β
目的 观察慢性氟中毒大鼠骨组织中骨保护素(OPG)、核因子κβ受体活化因子配体(RANKL)、核因子κβ受体活化因子(RANK)蛋白表达水平,探讨OPG/RAN KL/RANK系统与慢性氟中毒大鼠骨骼损伤的关系及丹蓝仙硼疗氟胶囊的拮抗作用.方法 将SD大鼠按体质量随机分为6组(组内雌雄各半):氟中毒组、高剂量药物组、中剂量药物组、低剂量药物组、对照组、硼砂(阳性药物对照)组,每组12只.对照组饮用自来水,其余5个实验组饮用含氟水(50 mg/L),而高、中、低剂量药物组另摄入丹蓝仙硼疗氟胶囊,剂量分别为0.8、O.4、O.2 g/kg,硼砂组另摄入硼砂,剂量为0.8 g/kg.6个月时用免疫组织化学方法检测OPG、RANKL、RANK蛋白在大鼠股骨干骺端的表达.结果 与对照组(173.79±5.23、174.17±5.O1、155.63±7.11)比较,氟中毒组大鼠股骨干骺端OPG、RANKL(156.83±5.80、157.74±6.70)表达增高,RANK(173.92±4.37)表达降低,差异有统计学意义(P均＜0.05).与氟中毒组比较,高、中剂量药物组OPG、RANKL(169.67±5.07、168.08±5.05,170.78±5.01、168.41±7.19)表达降低,RANK(162.12±4.24、166.69±5.78)表达增高,差异有统计学意义(P均＜O.05).与硼砂组(167.27±4.08、167.85±5.O1、166.14±3.95)比较,低剂量药物组OPG、RANKL(163.40±4.11、159.49±5.78)表达增高,RANK(171.54±8.06)表达降低,而高剂量药物组RANK(162.12±4.24)表达增高,差异有统计学意义(P均＜0.05).结论 慢性氟中毒可引起成骨与破骨活动均增强的骨转换增高状态,并可通过改变OPG/RANKL/RANK系统表达影响骨吸收的程度.丹蓝仙硼疗氟胶囊能通过OPG/RANKL/RANK系统影响骨重建,对氟致骨损伤有拮抗作用.
目的 觀察慢性氟中毒大鼠骨組織中骨保護素(OPG)、覈因子κβ受體活化因子配體(RANKL)、覈因子κβ受體活化因子(RANK)蛋白錶達水平,探討OPG/RAN KL/RANK繫統與慢性氟中毒大鼠骨骼損傷的關繫及丹藍仙硼療氟膠囊的拮抗作用.方法 將SD大鼠按體質量隨機分為6組(組內雌雄各半):氟中毒組、高劑量藥物組、中劑量藥物組、低劑量藥物組、對照組、硼砂(暘性藥物對照)組,每組12隻.對照組飲用自來水,其餘5箇實驗組飲用含氟水(50 mg/L),而高、中、低劑量藥物組另攝入丹藍仙硼療氟膠囊,劑量分彆為0.8、O.4、O.2 g/kg,硼砂組另攝入硼砂,劑量為0.8 g/kg.6箇月時用免疫組織化學方法檢測OPG、RANKL、RANK蛋白在大鼠股骨榦骺耑的錶達.結果 與對照組(173.79±5.23、174.17±5.O1、155.63±7.11)比較,氟中毒組大鼠股骨榦骺耑OPG、RANKL(156.83±5.80、157.74±6.70)錶達增高,RANK(173.92±4.37)錶達降低,差異有統計學意義(P均＜0.05).與氟中毒組比較,高、中劑量藥物組OPG、RANKL(169.67±5.07、168.08±5.05,170.78±5.01、168.41±7.19)錶達降低,RANK(162.12±4.24、166.69±5.78)錶達增高,差異有統計學意義(P均＜O.05).與硼砂組(167.27±4.08、167.85±5.O1、166.14±3.95)比較,低劑量藥物組OPG、RANKL(163.40±4.11、159.49±5.78)錶達增高,RANK(171.54±8.06)錶達降低,而高劑量藥物組RANK(162.12±4.24)錶達增高,差異有統計學意義(P均＜0.05).結論 慢性氟中毒可引起成骨與破骨活動均增彊的骨轉換增高狀態,併可通過改變OPG/RANKL/RANK繫統錶達影響骨吸收的程度.丹藍仙硼療氟膠囊能通過OPG/RANKL/RANK繫統影響骨重建,對氟緻骨損傷有拮抗作用.
목적 관찰만성불중독대서골조직중골보호소(OPG)、핵인자κβ수체활화인자배체(RANKL)、핵인자κβ수체활화인자(RANK)단백표체수평,탐토OPG/RAN KL/RANK계통여만성불중독대서골격손상적관계급단람선붕료불효낭적길항작용.방법 장SD대서안체질량수궤분위6조(조내자웅각반):불중독조、고제량약물조、중제량약물조、저제량약물조、대조조、붕사(양성약물대조)조,매조12지.대조조음용자래수,기여5개실험조음용함불수(50 mg/L),이고、중、저제량약물조령섭입단람선붕료불효낭,제량분별위0.8、O.4、O.2 g/kg,붕사조령섭입붕사,제량위0.8 g/kg.6개월시용면역조직화학방법검측OPG、RANKL、RANK단백재대서고골간후단적표체.결과 여대조조(173.79±5.23、174.17±5.O1、155.63±7.11)비교,불중독조대서고골간후단OPG、RANKL(156.83±5.80、157.74±6.70)표체증고,RANK(173.92±4.37)표체강저,차이유통계학의의(P균＜0.05).여불중독조비교,고、중제량약물조OPG、RANKL(169.67±5.07、168.08±5.05,170.78±5.01、168.41±7.19)표체강저,RANK(162.12±4.24、166.69±5.78)표체증고,차이유통계학의의(P균＜O.05).여붕사조(167.27±4.08、167.85±5.O1、166.14±3.95)비교,저제량약물조OPG、RANKL(163.40±4.11、159.49±5.78)표체증고,RANK(171.54±8.06)표체강저,이고제량약물조RANK(162.12±4.24)표체증고,차이유통계학의의(P균＜0.05).결론 만성불중독가인기성골여파골활동균증강적골전환증고상태,병가통과개변OPG/RANKL/RANK계통표체영향골흡수적정도.단람선붕료불효낭능통과OPG/RANKL/RANK계통영향골중건,대불치골손상유길항작용.
Objective To observe the expression of osteoprotegerin (OPG), receptor activator of nuclear factor κβ ligand(RANKL) and receptor activator of nuclear factor κβ (RANK) in bone tissue of rats with chronic fluorosis and to explore the relation between OPG/RANKL/RANK system and bone damage in chronic fluoride poisoning rat and the antagonism effects of Danlan Xianpeng capsule. Methods SD rats were randomly divided into six groups according to body weight (equal male and female in each group): fluorosis group, high dose drug group, medium dose drug group, low dose drug group, control group, borax group(positive control), 12 rats in each group. The control group drank tap water and the remaining 5 experimental groups consumed 50 mg/L fluoride water, and high, medium and low doses drug group took Danlan Xianpeng capsule at doses of 0.8,0.4,0.2 g/kg,borax group took borax at dose of 0.8 g/kg. OPG, RANKL, RANK protein in rat tibial metaphysis was detected by immunohistochemistry at the 6 month. Results Compared with the control group(173.79 ± 5.23, 174.17 ± 5.01,155.63 ± 7.11), the expressions of OPG, RANKL were increased and the expression of RANK was decreased in fluorosis group(156.83 ± 5.80, 157.74 ± 6.70, 173.92 ± 4.37), the difference was statistically significant (all P ＜ 0.05). Compared with the fluorosis group, the expression of OPG and RANKL were decreased and the expression of RANK was increased in high-dose drug group, middle-dose drug group(169.67±5.07, 168.08 ± 5.05,162.12 ± 4.24, 170.78 ± 5.01, 168.41 ± 7.19, 166.69 ± 5.78, all P ＜ 0.05). Compared with the borax group (167.27 ± 4.08, 167.85 ± 5.01, 166.14 ± 3.95), the expression of OPG and RANKL was increased in the low-dose drug group (163.40 ± 4.11, 159.49 ± 5.78), the expression of RANK was increased in the high-dose drug group (162.12 ± 4.24) and decreased in the low-dose drug group(171.54 ± 8.06), the difference was statistically significant (all P ＜ 0.05). Conclusions Chronic fluoride poisoning can cause increased bone turnover and enhance the activity of osteoelastic absorption by increasing RANKL. Danlan Xianpeng capsule can affect bone remodeling through the OPG/RANKL/RANK system, and antagonises bone damage caused by fluoride.
