广东药学院学报
廣東藥學院學報
엄동약학원학보
ACADEMIC JOURNAL OF GUANGDONG COLLEGE OF PHARMACY
2014年
4期
463-466
,共4页
贾欢欢%卢丽%陈珺%杨国柱%陆幸妍%吴玉娥%张钰%李青南
賈歡歡%盧麗%陳珺%楊國柱%陸倖妍%吳玉娥%張鈺%李青南
가환환%로려%진군%양국주%륙행연%오옥아%장옥%리청남
高盐饮食%第五腰椎骨%成骨细胞%破骨细胞%骨形态计量学
高鹽飲食%第五腰椎骨%成骨細胞%破骨細胞%骨形態計量學
고염음식%제오요추골%성골세포%파골세포%골형태계량학
high salt diet%fifth lumbar vertebra%osteoblast%osteoclast%bone histomorphometry
目的:研究高盐饮食对雄性大鼠腰椎松质骨的影响及其机理。方法选择5周龄SD雄性大鼠24只随机分为2组,分别饲喂不同钠盐比例的鼠粮,正常组含NaCl 2.6 g/kg,高盐饮食组含NaCl 20 g/kg,连续喂养60 d。实验结束,取第5腰椎骨( LV5)松质骨进行骨形态计量学分析。结果静态参数:高盐组腰椎骨骨小梁面积百分数、骨小梁厚度均低于正常组(P<0.05);而骨小梁分离度大于正常组(P<0.05);骨小梁数量两组差异无统计学意义。动态参数:高盐组腰椎骨荧光周长百分数显著低于正常组(P<0.01);而骨形成率( BFR/TV、BFR/BS)及成骨细胞数目也低于正常组( P<0.05);骨矿化沉积率、骨形成率BFR/BV及破骨细胞数目差异无统计学意义。结论高盐饮食可导致腰椎骨量减少,骨结构变差,其机理主要是高盐导致骨形成减少,而不影响骨吸收,最终使骨吸收大于骨形成。
目的:研究高鹽飲食對雄性大鼠腰椎鬆質骨的影響及其機理。方法選擇5週齡SD雄性大鼠24隻隨機分為2組,分彆飼餵不同鈉鹽比例的鼠糧,正常組含NaCl 2.6 g/kg,高鹽飲食組含NaCl 20 g/kg,連續餵養60 d。實驗結束,取第5腰椎骨( LV5)鬆質骨進行骨形態計量學分析。結果靜態參數:高鹽組腰椎骨骨小樑麵積百分數、骨小樑厚度均低于正常組(P<0.05);而骨小樑分離度大于正常組(P<0.05);骨小樑數量兩組差異無統計學意義。動態參數:高鹽組腰椎骨熒光週長百分數顯著低于正常組(P<0.01);而骨形成率( BFR/TV、BFR/BS)及成骨細胞數目也低于正常組( P<0.05);骨礦化沉積率、骨形成率BFR/BV及破骨細胞數目差異無統計學意義。結論高鹽飲食可導緻腰椎骨量減少,骨結構變差,其機理主要是高鹽導緻骨形成減少,而不影響骨吸收,最終使骨吸收大于骨形成。
목적:연구고염음식대웅성대서요추송질골적영향급기궤리。방법선택5주령SD웅성대서24지수궤분위2조,분별사위불동납염비례적서량,정상조함NaCl 2.6 g/kg,고염음식조함NaCl 20 g/kg,련속위양60 d。실험결속,취제5요추골( LV5)송질골진행골형태계량학분석。결과정태삼수:고염조요추골골소량면적백분수、골소량후도균저우정상조(P<0.05);이골소량분리도대우정상조(P<0.05);골소량수량량조차이무통계학의의。동태삼수:고염조요추골형광주장백분수현저저우정상조(P<0.01);이골형성솔( BFR/TV、BFR/BS)급성골세포수목야저우정상조( P<0.05);골광화침적솔、골형성솔BFR/BV급파골세포수목차이무통계학의의。결론고염음식가도치요추골량감소,골결구변차,기궤리주요시고염도치골형성감소,이불영향골흡수,최종사골흡수대우골형성。
Objective To study the effect and mechanism of high salt diet on lumbar bone in male rats. Methods Twenty-four,5-week old,male SD rats were divided into 2 groups,including the normal group(NS,2.6 g/kg NaCl) and the high salt diet group(HS,20 g/kg NaCl). After 60 days feed,the fifth lumbar vertebra(LV5) was taken for bone histomorphometry. Results Trabecular area percentage and bone trabecular thickness were significantly lower in the HS group when compared with those in the NS group. Trabecular separation was significantly increased in the HS group. However,no significant difference was found in bone trabecular number in two groups. Compared with the NS group,percent labeled perimeter,bone formation rate and the osteoblasts number were significantly lower in HS-treated rats. But, no significant difference was found in bone mineralization sedimentary rate, bone formation rate BFRS/BV and number of osteoclasts in two groups. Conclusion High salt diet can lead to reduced bone mass and bone structure variation,which mechanism may be related to the inhibition of bone formation,without affecting the bone absorption.