中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2014年
10期
735-738
,共4页
朱锦灿%陈小宇%刘成成%祝爱珍%刘善淘%刘革修
硃錦燦%陳小宇%劉成成%祝愛珍%劉善淘%劉革脩
주금찬%진소우%류성성%축애진%류선도%류혁수
辐射%脂肪细胞%骨髓微环境%红景天苷
輻射%脂肪細胞%骨髓微環境%紅景天苷
복사%지방세포%골수미배경%홍경천감
Radiation%Adipocyte%Bone marrow microenvironment%Salidroside
目的 探讨红景天苷抑制辐射诱导小鼠骨髓脂肪化、促进辐射后造血恢复的情况,并研究其可能的机制.方法 取6~7周龄健康BALB/c小鼠按随机数字表法分为健康对照组、单纯照射组、药物干预组,每组各20只.辐射对照组和实验组均给予6.0 Gy 60Co γ射线辐射处理,实验组于辐射后12 h腹腔注射红景天苷(30 mg·kg-1·d-1)至照后8d,辐射对照组腹腔注射等体积生理盐水.辐射后14 d观察小鼠的一般情况、体重变化、外周血象,并取股骨制作骨髓切片观察骨髓病理改变,测定脂肪细胞面积,分离骨髓单个核细胞后提取总RNA,荧光定量PCR(q-PCR)检测PPAR-γ和FABP4 mRNA的相对表达量.结果 单纯照射组小鼠在照射后均出现外周血白细胞降低、血小板减低,骨髓脂肪细胞过度增生,骨髓有核细胞减少等骨髓造血抑制改变.与单纯照射组小鼠比较,红景天苷能改善照射后小鼠一般情况,并通过抑制PPAR-γ、FABP4的表达(t=8.64、13.19,P<0.05),抑制骨髓脂肪细胞的过度增生,减少脂肪空泡面积(t=13.31,P<0.05);照后7d,药物干预组小鼠外周血白细胞计数高于单纯照射组(t =5.80,P<0.05);照后14 d,药物干预组小鼠外周血白细胞计数较单纯照射组及照后7d药物干预组小鼠外周血白细胞计数均有增高(t=13.78、7.54,P <0.05),同时血红蛋白较单纯照射组高(t=14.66,P<0.05).结论 红景天苷能抑制急性辐射损伤小鼠骨髓脂肪细胞生成,调节骨髓微环境,从而促进辐射损伤后小鼠造血恢复.
目的 探討紅景天苷抑製輻射誘導小鼠骨髓脂肪化、促進輻射後造血恢複的情況,併研究其可能的機製.方法 取6~7週齡健康BALB/c小鼠按隨機數字錶法分為健康對照組、單純照射組、藥物榦預組,每組各20隻.輻射對照組和實驗組均給予6.0 Gy 60Co γ射線輻射處理,實驗組于輻射後12 h腹腔註射紅景天苷(30 mg·kg-1·d-1)至照後8d,輻射對照組腹腔註射等體積生理鹽水.輻射後14 d觀察小鼠的一般情況、體重變化、外週血象,併取股骨製作骨髓切片觀察骨髓病理改變,測定脂肪細胞麵積,分離骨髓單箇覈細胞後提取總RNA,熒光定量PCR(q-PCR)檢測PPAR-γ和FABP4 mRNA的相對錶達量.結果 單純照射組小鼠在照射後均齣現外週血白細胞降低、血小闆減低,骨髓脂肪細胞過度增生,骨髓有覈細胞減少等骨髓造血抑製改變.與單純照射組小鼠比較,紅景天苷能改善照射後小鼠一般情況,併通過抑製PPAR-γ、FABP4的錶達(t=8.64、13.19,P<0.05),抑製骨髓脂肪細胞的過度增生,減少脂肪空泡麵積(t=13.31,P<0.05);照後7d,藥物榦預組小鼠外週血白細胞計數高于單純照射組(t =5.80,P<0.05);照後14 d,藥物榦預組小鼠外週血白細胞計數較單純照射組及照後7d藥物榦預組小鼠外週血白細胞計數均有增高(t=13.78、7.54,P <0.05),同時血紅蛋白較單純照射組高(t=14.66,P<0.05).結論 紅景天苷能抑製急性輻射損傷小鼠骨髓脂肪細胞生成,調節骨髓微環境,從而促進輻射損傷後小鼠造血恢複.
목적 탐토홍경천감억제복사유도소서골수지방화、촉진복사후조혈회복적정황,병연구기가능적궤제.방법 취6~7주령건강BALB/c소서안수궤수자표법분위건강대조조、단순조사조、약물간예조,매조각20지.복사대조조화실험조균급여6.0 Gy 60Co γ사선복사처리,실험조우복사후12 h복강주사홍경천감(30 mg·kg-1·d-1)지조후8d,복사대조조복강주사등체적생리염수.복사후14 d관찰소서적일반정황、체중변화、외주혈상,병취고골제작골수절편관찰골수병리개변,측정지방세포면적,분리골수단개핵세포후제취총RNA,형광정량PCR(q-PCR)검측PPAR-γ화FABP4 mRNA적상대표체량.결과 단순조사조소서재조사후균출현외주혈백세포강저、혈소판감저,골수지방세포과도증생,골수유핵세포감소등골수조혈억제개변.여단순조사조소서비교,홍경천감능개선조사후소서일반정황,병통과억제PPAR-γ、FABP4적표체(t=8.64、13.19,P<0.05),억제골수지방세포적과도증생,감소지방공포면적(t=13.31,P<0.05);조후7d,약물간예조소서외주혈백세포계수고우단순조사조(t =5.80,P<0.05);조후14 d,약물간예조소서외주혈백세포계수교단순조사조급조후7d약물간예조소서외주혈백세포계수균유증고(t=13.78、7.54,P <0.05),동시혈홍단백교단순조사조고(t=14.66,P<0.05).결론 홍경천감능억제급성복사손상소서골수지방세포생성,조절골수미배경,종이촉진복사손상후소서조혈회복.
Objective To investigate the potential and underlying molecular mechanism of salidroside in ameliorating radiation-induced bone marrow adipogenesis and stimulating hematopoiesis.Methods The female BALB/c mice aged 6-7 weeks were randomly divided into normal control group,radiation group and salidroside group.The radiation group and salidroside group were irradiated with 6.0 Gy of 60Co γ-rays.The salidroside group was intraperitoneally injected with 30 mg· kg-1 · d-1 salidroside at 12 h and then every day until 8th d after radiation.The normal control group and radiation group were treated with equal volume of saline as control of salidroside.At 14 d after radiation,the mice weight,peripheral blood count,femur bone marrow histology,and the proportion of adipocyte area were measured,and the expressions of PPAR-γ and FABP4 were detected by q-PCR.Results After irradiation,the numbers of white blood cells,hemoglobin and platelet in peripheral blood were reduced obviously,and the percentage of adipocyte area was increased significantly.Compared with mice in the radiation group,salidroside inhibited adipogenesis and reduced the proportion of adipocyte area (t =13.31,P < 0.05) by reducing the expressions of PPAR-γ and FABP4 (t =8.64,13.19,P < 0.05).The number of white blood cells was partly recovered at 7 d after irradiation (t =5.80,P < 0.05).Both white blood cells and hemoglobinin in peripheral blood of the salidroside group were higher than those in the radiation group at 14 d after irradiation.Conclusions Salidroside could inhibit radiation-induced bone marrow adipogenesis and regulate bone marrow microenvironment,thereby promotes hematopoietic recovery in mice after radiation injury.