CAJ | 학술논문

目的：观察骨碎补总黄酮对去卵巢大鼠骨组织Ⅰ型胶原表达及骨代谢的影响。方法：雌性SD大鼠40只，月龄10个月，随机分为实验组、空白对照组、模型组和阳性对照组，每组10只。除空白对照组外，其余各组均切除双侧卵巢制作骨质疏松模型。造模后第8天开始药物干预，实验组予以骨碎补总黄酮浓缩液2 mL灌胃，阳性对照组予以倍美力混悬剂2 mL灌胃；空白对照组和模型组予以生理盐水2 mL灌胃；均每日1次。药物干预6个月后，比较各组大鼠骨密度、尿脱氧吡啶啉/尿肌酐比值、Ⅰ型胶原氨基末端肽/尿肌酐比值及血清Ⅰ型前胶原氨基端前肽含量；并检测各组大鼠骨组织中Ⅰ型胶原mRNA的表达。结果：药物干预6个月后，各组大鼠间骨密度值比较，差异有统计学意义[（0.287±0.017）g·cm-2，（0.362±0.031）g·cm-2，（0.207±0.008）g ·cm-2，（0.291±0.015）g·cm-2；F＝104.317，P＝0.000）]；实验组低于空白对照组（P＝0.000），高于模型组（P＝0.000），但与阳性对照组比较，差异无统计学意义（P＝0.584）；空白对照组高于模型组和阳性对照组（P＝0.000，P＝0.000）；模型组低于阳性对照组（P＝0.000）。各组间尿脱氧吡啶啉/尿肌酐比值（3.381±0.202，2.462±0.310，4.526±0.243，3.232±0.191）、Ⅰ型胶原氨基末端肽/尿肌酐比值（10.901±1.265，8.638±1.036，13.392±1.959，10.516±1.362）及血清Ⅰ型前胶原氨基端前肽含量[（232.081±28.452）μg·mL-1，（184.443±19.250）μg·mL-1，（283.262±33.628）μg·mL-1，（238.861±26.685）μg·mL-1]比较，差异均有统计学意义（F＝124.841，P＝0.000；F＝18.277，P＝0.000；F＝21.648，P＝0.000）；实验组高于空白对照组，差异均有统计学意义（P＝0.000，P＝0.000，P＝0.000）；实验组低于模型组，差异有统计学意义（P＝0.000，P＝0.003，P＝0.002）；实验组与阳性对照组比较，差异均无统计学意义（ P＝0.107，P＝0.521，P＝0.589）；空白对照组低于模型组和阳性对照组，差异有统计学意义（P＝0.000，P＝0.000，P＝0.000；P＝0.000，P＝0.003，P＝0.000）；模型组高于阳性对照组，差异均有统计学意义（P＝0.000，P＝0.001，P＝0.004）。空白对照组大鼠骨组织Ⅰ型胶原mRNA表达最强；模型组大鼠骨组织Ⅰ型胶原mRNA表达呈阴性或低表达；实验组大鼠骨组织Ⅰ型胶原mRNA表达水平与阳性对照组接近，较模型组强。结论：骨碎补总黄酮能增强去卵巢大鼠骨组织Ⅰ型胶原的表达，降低骨转换率，增加骨密度；这可能是骨碎补总黄酮防治骨质疏松症的机制之一。目的：觀察骨碎補總黃酮對去卵巢大鼠骨組織Ⅰ型膠原錶達及骨代謝的影響。方法：雌性SD大鼠40隻，月齡10箇月，隨機分為實驗組、空白對照組、模型組和暘性對照組，每組10隻。除空白對照組外，其餘各組均切除雙側卵巢製作骨質疏鬆模型。造模後第8天開始藥物榦預，實驗組予以骨碎補總黃酮濃縮液2 mL灌胃，暘性對照組予以倍美力混懸劑2 mL灌胃；空白對照組和模型組予以生理鹽水2 mL灌胃；均每日1次。藥物榦預6箇月後，比較各組大鼠骨密度、尿脫氧吡啶啉/尿肌酐比值、Ⅰ型膠原氨基末耑肽/尿肌酐比值及血清Ⅰ型前膠原氨基耑前肽含量；併檢測各組大鼠骨組織中Ⅰ型膠原mRNA的錶達。結果：藥物榦預6箇月後，各組大鼠間骨密度值比較，差異有統計學意義[（0.287±0.017）g·cm-2，（0.362±0.031）g·cm-2，（0.207±0.008）g ·cm-2，（0.291±0.015）g·cm-2；F＝104.317，P＝0.000）]；實驗組低于空白對照組（P＝0.000），高于模型組（P＝0.000），但與暘性對照組比較，差異無統計學意義（P＝0.584）；空白對照組高于模型組和暘性對照組（P＝0.000，P＝0.000）；模型組低于暘性對照組（P＝0.000）。各組間尿脫氧吡啶啉/尿肌酐比值（3.381±0.202，2.462±0.310，4.526±0.243，3.232±0.191）、Ⅰ型膠原氨基末耑肽/尿肌酐比值（10.901±1.265，8.638±1.036，13.392±1.959，10.516±1.362）及血清Ⅰ型前膠原氨基耑前肽含量[（232.081±28.452）μg·mL-1，（184.443±19.250）μg·mL-1，（283.262±33.628）μg·mL-1，（238.861±26.685）μg·mL-1]比較，差異均有統計學意義（F＝124.841，P＝0.000；F＝18.277，P＝0.000；F＝21.648，P＝0.000）；實驗組高于空白對照組，差異均有統計學意義（P＝0.000，P＝0.000，P＝0.000）；實驗組低于模型組，差異有統計學意義（P＝0.000，P＝0.003，P＝0.002）；實驗組與暘性對照組比較，差異均無統計學意義（ P＝0.107，P＝0.521，P＝0.589）；空白對照組低于模型組和暘性對照組，差異有統計學意義（P＝0.000，P＝0.000，P＝0.000；P＝0.000，P＝0.003，P＝0.000）；模型組高于暘性對照組，差異均有統計學意義（P＝0.000，P＝0.001，P＝0.004）。空白對照組大鼠骨組織Ⅰ型膠原mRNA錶達最彊；模型組大鼠骨組織Ⅰ型膠原mRNA錶達呈陰性或低錶達；實驗組大鼠骨組織Ⅰ型膠原mRNA錶達水平與暘性對照組接近，較模型組彊。結論：骨碎補總黃酮能增彊去卵巢大鼠骨組織Ⅰ型膠原的錶達，降低骨轉換率，增加骨密度；這可能是骨碎補總黃酮防治骨質疏鬆癥的機製之一。
목적：관찰골쇄보총황동대거란소대서골조직Ⅰ형효원표체급골대사적영향。방법：자성SD대서40지，월령10개월，수궤분위실험조、공백대조조、모형조화양성대조조，매조10지。제공백대조조외，기여각조균절제쌍측란소제작골질소송모형。조모후제8천개시약물간예，실험조여이골쇄보총황동농축액2 mL관위，양성대조조여이배미력혼현제2 mL관위；공백대조조화모형조여이생리염수2 mL관위；균매일1차。약물간예6개월후，비교각조대서골밀도、뇨탈양필정람/뇨기항비치、Ⅰ형효원안기말단태/뇨기항비치급혈청Ⅰ형전효원안기단전태함량；병검측각조대서골조직중Ⅰ형효원mRNA적표체。결과：약물간예6개월후，각조대서간골밀도치비교，차이유통계학의의[（0.287±0.017）g·cm-2，（0.362±0.031）g·cm-2，（0.207±0.008）g ·cm-2，（0.291±0.015）g·cm-2；F＝104.317，P＝0.000）]；실험조저우공백대조조（P＝0.000），고우모형조（P＝0.000），단여양성대조조비교，차이무통계학의의（P＝0.584）；공백대조조고우모형조화양성대조조（P＝0.000，P＝0.000）；모형조저우양성대조조（P＝0.000）。각조간뇨탈양필정람/뇨기항비치（3.381±0.202，2.462±0.310，4.526±0.243，3.232±0.191）、Ⅰ형효원안기말단태/뇨기항비치（10.901±1.265，8.638±1.036，13.392±1.959，10.516±1.362）급혈청Ⅰ형전효원안기단전태함량[（232.081±28.452）μg·mL-1，（184.443±19.250）μg·mL-1，（283.262±33.628）μg·mL-1，（238.861±26.685）μg·mL-1]비교，차이균유통계학의의（F＝124.841，P＝0.000；F＝18.277，P＝0.000；F＝21.648，P＝0.000）；실험조고우공백대조조，차이균유통계학의의（P＝0.000，P＝0.000，P＝0.000）；실험조저우모형조，차이유통계학의의（P＝0.000，P＝0.003，P＝0.002）；실험조여양성대조조비교，차이균무통계학의의（ P＝0.107，P＝0.521，P＝0.589）；공백대조조저우모형조화양성대조조，차이유통계학의의（P＝0.000，P＝0.000，P＝0.000；P＝0.000，P＝0.003，P＝0.000）；모형조고우양성대조조，차이균유통계학의의（P＝0.000，P＝0.001，P＝0.004）。공백대조조대서골조직Ⅰ형효원mRNA표체최강；모형조대서골조직Ⅰ형효원mRNA표체정음성혹저표체；실험조대서골조직Ⅰ형효원mRNA표체수평여양성대조조접근，교모형조강。결론：골쇄보총황동능증강거란소대서골조직Ⅰ형효원적표체，강저골전환솔，증가골밀도；저가능시골쇄보총황동방치골질소송증적궤제지일。
Objective:To observe the effect of drynaria fortunei total flavonoids on collagen typeⅠ( COL-Ⅰ)expression in bone tis-sue and bone metabolism in the ovariectomized rats. Methods:Forty ten-month-old female SD rats were randomly divided into experi-mental group,blank control group,model group and positive control group,10 rats in each group. The osteoporosis rat models were built by bilateral ovariectomy in experimental group,model group and positive control group. The drug intervention were carried out from the 8th day after modeling. The rats in the experimental group were intragastric administrated with concentrated solution of drynaria fortunei total fla-vonoids(2 mL qd),the rats in the positive control group were intragastric administrated with Premarin suspensions(2 mL qd),while the others in the blank control group and model group were intragastric administrated with normal saline(2 mL qd). After 6 months of drug in-tervention,bone density,urine content ratio of deoxy pyridinoline( DPD)to creatinine( Cre),urine content ratio of N-telopeptide of typeⅠcollagen( NTx)to creatinine( Cre)and serum content of amino-terminal propeptide of typeⅠ procollagen( PINP)were detected and com-pared between the 4 groups. Meanwhile,the COL-ⅠmRNA expression in bone tissues were detected. Results:After drug intervening for 6 months,there were statistical differences in the bone density between the 4 groups(0. 287+/-0. 017,0. 362+/-0. 031,0. 207+/-0. 008, 0. 291 +/-0. 015 g/cm( 2 );F =104. 317,P =0. 000 ). Further comparison indicated that the bone density value of experimental group was lower than that of the blank control group(P=0. 000)and higher than that of model group(P=0. 000),while there was no sta-tistical difference in the bone density value between the experimental group and positive control group(P=0. 584). The bone density value of the blank control group was higher than that of model group and positive control group(P=0. 000,P=0. 000),while the bone density value of the model group was lower than that of positive control group(P=0. 000). There were statistical differences in the urine content ratio of DPD to Cre(3. 381+/-0. 202,2. 462+/-0. 310,4. 526+/-0. 243,3. 232+/-0. 191),the urine content ratio of NTx to Cre(10. 901+/-1. 265,8. 638+/-1. 036,13. 392 +/-1. 959,10. 516 +/-1. 362)and the serum content of PINP(232. 081 +/ -28. 452,184. 443 +/-19. 250,283. 262+/-33. 628,238. 861+/-26. 685 μg/mL)between the 4 groups( F=124. 841,P=0. 000;F=18. 277,P=0. 000;F=21. 648,P=0. 000). The values of these bone metabolism indexes were higher in the experimental group compared with the blank control group(P=0. 000,P=0. 000,P=0. 000)and were lower in the experimental group compared with the model group(P=0. 000,P=0. 003, P=0. 002). There were no statistical differences in the values between the experimental group and the positive control group( P=0. 107, P=0. 521,P=0. 589). The values of the blank control group were lower than those of the model group and the positive control group(P=0. 000,P=0. 000,P=0. 000;P=0. 000,P=0. 003,P=0. 000). The values of the model group were higher than those of the positive con-trol group(P=0. 000,P=0. 001,P=0. 004). Strong-positive expression of COL-ⅠmRNA in bone tissues was found in the blank con-trol group,while negative or low expression of COL-ⅠmRNA was found in the model group. The experimental group was similar to the positive control group and surpassed the model group in the expression of COL-ⅠmRNA in bone tissues. Conclusion:The drynaria fortu-nei total flavonoids can enhance the COL-Ⅰexpression in bone tissues of ovariectomized rats and reduce the bone turnover rate and in-crease the bone density,which may be one of the mechanisms for drynaria fortunei total flavonoids in the prevention of osteoporosis.