CAJ | 학술논문

目的：探讨半枝莲总黄酮(TFSB)对高脂饲养ApoE基因缺陷(ApoE-/-)小鼠在动脉粥样硬化(AS)病变形成早期抑制AS的作用及其分子机制。方法11周龄♂ApoE-/-小鼠40只,随机分为模型组、TFSB低、中、高剂量组、辛伐他汀组,每组8只。取C57BL/6J小鼠8只作为正常对照组。均给予高脂饲养4周后给药,8周后全部处死, HE染色观察主动脉形态学变化,血液流变仪测血浆黏度、全血黏度(低切、高切),温氏法测红细胞比容。全自动生化分析仪检测血清TG、TC、HDL-C、LDL-C表达水平, ELISA法检测血清磷脂转运蛋白(PLTP)及维生素E(VE)的表达水平。Westernblot法检测各组小鼠肝脏PLTP蛋白表达水平及法尼酯衍生物X受体(FXR)表达水平。结果模型组造模成功；TFSB各剂量组对模型小鼠主动脉AS形态学有改善作用,可明显降低AS模型小鼠血清TG、TC、LDL-C水平,升高HDL-C水平,与模型组比较,差异均具有显著性(P<0．05或P<0．01)；TFSB各剂量组可明显降低AS模型鼠的红细胞比容、血浆黏度及全血黏度(低切、高切),且与模型组相比,差异均有显著性(P<0．01)；TFSB各剂量组血清PLTP表达水平较模型组明显减少,差异均有显著性(P<0．01),且PLTP与VE水平呈负相关(r=-0．675, P<0．01)；与模型组相比, TFSB中、高剂量组能够明显抑制肝脏PLTP及FXR蛋白表达水平(P<0．01)。结论TFSB可能通过调节ApoE-/-小鼠FXR水平,从而调节PLTP 水平、升高VE 水平、调节血脂、改善血液流变学及减少小鼠的AS 损伤,进而发挥抗AS 的作用。
목적：탐토반지련총황동(TFSB)대고지사양ApoE기인결함(ApoE-/-)소서재동맥죽양경화(AS)병변형성조기억제AS적작용급기분자궤제。방법11주령♂ApoE-/-소서40지,수궤분위모형조、TFSB저、중、고제량조、신벌타정조,매조8지。취C57BL/6J소서8지작위정상대조조。균급여고지사양4주후급약,8주후전부처사, HE염색관찰주동맥형태학변화,혈액류변의측혈장점도、전혈점도(저절、고절),온씨법측홍세포비용。전자동생화분석의검측혈청TG、TC、HDL-C、LDL-C표체수평, ELISA법검측혈청린지전운단백(PLTP)급유생소E(VE)적표체수평。Westernblot법검측각조소서간장PLTP단백표체수평급법니지연생물X수체(FXR)표체수평。결과모형조조모성공；TFSB각제량조대모형소서주동맥AS형태학유개선작용,가명현강저AS모형소서혈청TG、TC、LDL-C수평,승고HDL-C수평,여모형조비교,차이균구유현저성(P<0．05혹P<0．01)；TFSB각제량조가명현강저AS모형서적홍세포비용、혈장점도급전혈점도(저절、고절),차여모형조상비,차이균유현저성(P<0．01)；TFSB각제량조혈청PLTP표체수평교모형조명현감소,차이균유현저성(P<0．01),차PLTP여VE수평정부상관(r=-0．675, P<0．01)；여모형조상비, TFSB중、고제량조능구명현억제간장PLTP급FXR단백표체수평(P<0．01)。결론TFSB가능통과조절ApoE-/-소서FXR수평,종이조절PLTP 수평、승고VE 수평、조절혈지、개선혈액류변학급감소소서적AS 손상,진이발휘항AS 적작용。
Aim To observe the effects of the total fla-vonoids of scutellaria barbataon ( TFSB ) on high-fat <br> feeding ApoE gene deficiency mice in early atheroscle-rosis ( AS ) and its underlying mechanisms. Methods <br> 40 ApoE-/ -male mice were divided into five groups:model group, SIM group and L-TFSB, M-TFSB, H-TFSB group, 5 C57BL/6J mice were selected as nor-mal control group. All mice in experimental group were fed with high-lipid diet for 4 weeks and all mice were killed after 8 weeks. H&E staining was used to observe morphology of aorta. Blood rheometer was used to ex-amine plasm viscosity and whole blood viscosity. Fully automatic biochemical analyser was used to detect the serum levels of TG, TC, LDL-C and HDL-C. The ex-pression levels of PLTP and VE in serum were meas-ured by ELISA. The expression levels of PLTP and FXR in liver were examined by Western blot. Results The model was established successfully. TFSB groups could improve the aorta AS morphology of model mice and significantly reduce the serum levels of TG, TC and LDL-C, while increase the level of HDL-C ( P<0. 05 or P<0. 01 ) . TFSB groups could decrease the <br> hematocrit value, plasma viscosity and whole blood vis-cosity of AS model mice significantly and had statistical significance when compared with model group ( P <0. 01 ) . The expression levels of PLTP of serum were reduced significantly when compared with model group ( P <0. 01 ) . We also found that the expression of PLTP was in negative correlation with VE ( r = -0. 675,P<0. 01). M-TFSB and H-TFSB group could decrease the expressions of PLTP and FXR of liver when compared with model group ( P <0. 01 ) . Con-clusion TFSB may exert its anti-AS effect partly through inhibiting the levels of FXR and PLTP of ApoE-/ -mice, increasing the level of VE, regulating blood lipids, improving blood rheology and reducing the damage of AS in mice.