CAJ | 학술논문

生脉散/药理学%脂多糖类/副作用%肝功能衰竭/代谢/中药疗法%内毒素类/代谢%肿瘤坏死因子α/代谢%白细胞介素1β/代谢%白细胞介素6/代谢%胞间黏附分子1/代谢生脈散/藥理學%脂多糖類/副作用%肝功能衰竭/代謝/中藥療法%內毒素類/代謝%腫瘤壞死因子α/代謝%白細胞介素1β/代謝%白細胞介素6/代謝%胞間黏附分子1/代謝
생맥산/약이학%지다당류/부작용%간공능쇠갈/대사/중약요법%내독소류/대사%종류배사인자α/대사%백세포개소1β/대사%백세포개소6/대사%포간점부분자1/대사
SHENGMAI POWDERS/PD%Lipopolysaccharides/AE%Liver failure/ME/ZD%Endotoxins/ME%Tumor necrosis factor-alpha/ME%Interleukin-1beta/ME%Interleukin-6/ME%Intercellular adhesion molecule-1/ME

目的探讨生脉散对慢性肝衰竭大鼠大肠杆菌脂多糖(LPS)诱导细胞因子水平的影响.方法采用CCl4混合液腹腔注射复制慢性肝衰竭大鼠模型,观察LPS诱导2 h后生脉散后对血清内毒素、细胞因子水平的影响.结果 CCl4混合液能明显增加大鼠血清IL-6[(64.50±18.79)pg/ml vs (4.79±0.57)pg/ml]、ICAM-1[(25100.00±5258.85)pg/ml vs (4215.50±942.79)pg/ml]和TNF-α[(17.55±2.39)pg/ml vs (10.92±5.02)pg/ml]水平(P＜0.05),但对血清LPS水平无明显影响[(0.058±0.007)EU/ml vs (0.040±0.002)EU/ml,P＞0.05];中药生脉散能显著降低CCl4慢性肝衰竭大鼠血清IL-6、ICAM-1和TNF-α水平[分别为(17.20±3.12)pg/ml、(9490.00±2725.78)pg/ml、(3.00±1.00)pg/ml,P＜0.05].LPS攻击2 h后能明显升高CCl4混合液大鼠血清LPS、TNF-α、IL-6、ICAM-1水平[分别为(0.501±0.019)EU/ml、(19750.00±9655.17)pg/ml、(5615.00±490.50)pg/ml、(41000.00±589.88)pg/ml,P＜0.01].结论在慢性肝衰竭模型中,LPS能增加TNF-α,IL-6和ICAM-1等炎症因子水平,中药生脉散可降低LPS水平,并抑制LPS诱导的炎症因子水平,阻断了炎性介质及LPS本身对机体的损伤.
목적 탐토생맥산대만성간쇠갈대서대장간균지다당(LPS)유도세포인자수평적영향.방법 채용CCl4혼합액복강주사복제만성간쇠갈대서모형,관찰LPS유도2 h후생맥산후대혈청내독소、세포인자수평적영향.결과 CCl4혼합액능명현증가대서혈청IL-6[(64.50±18.79)pg/ml vs (4.79±0.57)pg/ml]、ICAM-1[(25100.00±5258.85)pg/ml vs (4215.50±942.79)pg/ml]화TNF-α[(17.55±2.39)pg/ml vs (10.92±5.02)pg/ml]수평(P＜0.05),단대혈청LPS수평무명현영향[(0.058±0.007)EU/ml vs (0.040±0.002)EU/ml,P＞0.05];중약생맥산능현저강저CCl4만성간쇠갈대서혈청IL-6、ICAM-1화TNF-α수평[분별위(17.20±3.12)pg/ml、(9490.00±2725.78)pg/ml、(3.00±1.00)pg/ml,P＜0.05].LPS공격2 h후능명현승고CCl4혼합액대서혈청LPS、TNF-α、IL-6、ICAM-1수평[분별위(0.501±0.019)EU/ml、(19750.00±9655.17)pg/ml、(5615.00±490.50)pg/ml、(41000.00±589.88)pg/ml,P＜0.01].결론 재만성간쇠갈모형중,LPS능증가TNF-α,IL-6화ICAM-1등염증인자수평,중약생맥산가강저LPS수평,병억제LPS유도적염증인자수평,조단료염성개질급LPS본신대궤체적손상.
Objective To study the Sheng Mai San on the levels of cell factors induced by lipopolysaccharide in acute liver failure rats. Methods The models of chronic liver failure were constructed by injecting CCl4 in the abdomen of rats. The serum levels of lipopolysaccharide and cell factors were determined after treating with LPS and Sheng Mai San for 2 hours. Results The serum level of IL-6［(64.50±18.79)pg/ml vs (4.79±0.57)pg/ml］, ICAM-1［(25100.00±5258.85)pg/ml vs (4215.50±942.79)pg/ml］ and TNF-α［(17.55±2.39)pg/ml vs (10.92±5.02)pg/ml］ was increased by CCl4 (P＜0.05), but there is no effect on the serum level of LPS in rats ［(0.058±0.007)EU/ml vs (0.040±0.002)EU/ml,P＞0.05］. Sheng Mai San can significantly reduce the serum level of IL-6, ICAM-1 and TNF-α in rats with acute liver failure induced by CCl4 ［(17.20±3.12)pg/ml,(9490.00±2725.78)pg/ml,(3.00±1.00)pg/ml,P＜0.05］. After treating with LPS for 2 hours, the serum level of LPS, TNF-α, IL-6, ICAM-1 markedly increased ［(0.501±0.019)EU/ml,(19750.00±9655.17)pg/ml,(5615.00±490.50)pg/ml,(41000.00±589.88)pg/ml,P＜0.01］. Sheng Mai San could reduce the serum levels of LPS, TNF-α, IL-6, ICAM-1 and in rats with chronic liver failure (P＜0.01). Conclusions SD Rats in the state of chronic liver fail-ure, existing serious serum endotoxin, can induce the levels of cell factors by diversification inflammation reaction and. ShengMaiSan can regulating the levels of cell factors in rats with chronic liver failure.