CAJ | 학술논문

目的：探讨降脂合剂对高脂血症大鼠氧自由基代谢及低密度脂蛋白（LDL）氧化易感性的影响，阐明降脂合剂调节血脂的可能机制。方法：60只雄性Wistar大鼠随机等分为正常组，模型组，辛伐他汀组及降脂合剂高、中、低剂量组，每组10只。除正常组外，其余各组高脂饲料喂饲建立高脂血症大鼠模型，造模同时给药，正常组、模型组灌胃生理盐水2mL，辛伐他汀组灌胃7.2×10-4g·mL-1的辛伐他汀混悬溶液2mL，降脂合剂低、中、高剂量组分别灌胃0.25、0.5、1.0g·mL-1的中药煎剂2mL，1次/天，持续10周。造模结束所有动物均摘眼球取血，全自动生化分析仪测定大鼠血脂谱，血浆前列环素（PGI2）、血栓素A2（TXA2）含量，超氧化物歧化酶（SOD）和谷胱甘肽过氧化酶（GSH-Px）活性，分离LDL，测其氧化易感性。结果：与模型组比较，降脂合剂各剂量组预防用药后，血浆PGI2含量及PGI2/TXA2比值均不同程度升高（P<0.05或P<0.01），血清SOD、GSH-Px活性显著提高（P<0.01），高密度脂蛋白（HDL-C）均有不同程度的升高（P<0.05或P<0.01），胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）水平均明显减低（P<0.05或P<0.01）；与模型组比较，降脂合剂各剂量组LDL氧化延迟时间（LagTime）和最大氧化速率时间（Tmax）均明显延长（P约0.05或P约0.01）。结论：降脂合剂能通过增强抗氧化酶活性，调整PGI2与TXA2的平衡状态，纠正脂蛋白-胆固醇及自由基代谢紊乱等途径发挥调血脂作用，明显降低高脂血症大鼠LDL氧化易感性，从而防止动脉硬化的形成和发展，对血脂异常有较好的调节作用。
목적：탐토강지합제대고지혈증대서양자유기대사급저밀도지단백（LDL）양화역감성적영향，천명강지합제조절혈지적가능궤제。방법：60지웅성Wistar대서수궤등분위정상조，모형조，신벌타정조급강지합제고、중、저제량조，매조10지。제정상조외，기여각조고지사료위사건립고지혈증대서모형，조모동시급약，정상조、모형조관위생리염수2mL，신벌타정조관위7.2×10-4g·mL-1적신벌타정혼현용액2mL，강지합제저、중、고제량조분별관위0.25、0.5、1.0g·mL-1적중약전제2mL，1차/천，지속10주。조모결속소유동물균적안구취혈，전자동생화분석의측정대서혈지보，혈장전렬배소（PGI2）、혈전소A2（TXA2）함량，초양화물기화매（SOD）화곡광감태과양화매（GSH-Px）활성，분리LDL，측기양화역감성。결과：여모형조비교，강지합제각제량조예방용약후，혈장PGI2함량급PGI2/TXA2비치균불동정도승고（P<0.05혹P<0.01），혈청SOD、GSH-Px활성현저제고（P<0.01），고밀도지단백（HDL-C）균유불동정도적승고（P<0.05혹P<0.01），담고순（TC）、감유삼지（TG）、저밀도지단백（LDL-C）수평균명현감저（P<0.05혹P<0.01）；여모형조비교，강지합제각제량조LDL양화연지시간（LagTime）화최대양화속솔시간（Tmax）균명현연장（P약0.05혹P약0.01）。결론：강지합제능통과증강항양화매활성，조정PGI2여TXA2적평형상태，규정지단백-담고순급자유기대사문란등도경발휘조혈지작용，명현강저고지혈증대서LDL양화역감성，종이방지동맥경화적형성화발전，대혈지이상유교호적조절작용。
This study was aimed to discuss the effect of Jiang-Zhi (JZ) Mixture on oxygen free radical metabolism and low density lipoprotein (LDL) oxidative susceptibility and elucidate the possible mechanism of JZ Mixture regulating blood lipid. A total of 60 male Wistar rats were randomly divided into the normal group, model group, simvastatin group and JZ Mixture of high-, middle-, and low-dose groups, with 10 rats in each group. Except the normal group, rats in other groups were fed with high fat diet to establish the rat model of hyperlipidemia. Medication was used during modeling for prevention. Intragastric administration of physiological saline (2 mL) was given to rats in the normal group and model group. Intragastric administration of simvastatin suspension solution (7.2í10-4 g·mL-1, 2 mL) was given to rats in the simvastatin group. Intragastric administration of JZ Mixture (0.25, 0.5, 1.0 g·mL-1, 2 mL) was given to the JZ Mixture of high, middle, and low-dose groups, respectively. The medication was given once a day and continued for 10 weeks. Then, eyeball blood was abstracted at the end of modeling. The full automatic biochemical analyzer was used in the determination of serum lipid profile, plasma prostacyclin (PGI2) and thromboxane A2(TXA2) content, as well as superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px) activity. After separation of LDL, the susceptibility to oxidation was determined. The results showed that compared with the model group, after preventive treatment of JZ Mixture in each dose group, the plasma PGI2 content and PGI2/TXA2 ratio were increased to varying degrees (P < 0.05 or P < 0.01), the serum SOD, GSH-Px activity was significantly increased(P< 0.01). The high density lipoprotein(HDL-C) was increased to varying degrees(P < 0.05 or P < 0.01), and the cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL-C) levels were all obviously decreased (P<0.05 or P < 0.01) in JZ Mixture groups. Compared with the model group, Lag time and Tmax were significantly prolonged in all LZ Mixture groups with statistical differences ( P < 0.05 or P < 0.01). It was concluded that JZ Mixture can enhance the activity of antioxidant enzymes, adjust PGI2 and TXA2 balance, correct lipoprotein cholesterol and free radical metabolism to play effects of regulating blood lipid, and significantly reduce the susceptibility of LDL to oxidation among hyperlipidemia rats, so as to prevent the formation and development of arteriosclerosis. It has a better regulative effect on abnormal serum lipid.