中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2014年
10期
1452-1455,1456
,共5页
孙梦雯%胡世莲%殷实%严光
孫夢雯%鬍世蓮%慇實%嚴光
손몽문%호세련%은실%엄광
脑肠肽%酒精性肝损伤%氧自由基%TNF-α%IL-1β%MCP-1
腦腸肽%酒精性肝損傷%氧自由基%TNF-α%IL-1β%MCP-1
뇌장태%주정성간손상%양자유기%TNF-α%IL-1β%MCP-1
ghrelin%alcoholic liver injury%oxygen free radicals%TNF-α%IL-1β%MCP-1
目的:研究脑肠肽对小鼠酒精性肝损伤的保护作用。方法采用4周5%酒精饲料喂饲加5 g·kg-1的高剂量酒精灌胃诱导酒精性肝损伤模型,用分光光度法检测血清中ALT、AST和肝匀浆MDA、SOD、GSH-Px含量;Real-time PCR法检测肝脏中炎症细胞因子 TNF-α、IL-1β、IFN-γ、IL-6和MCP-1的表达。 HE染色检测肝脏病理改变。结果这种慢性酒精喂饲+单剂量大剂量酒精灌胃模式可明显诱导酒精性肝损伤,可导致明显的转氨酶升高、脂肪肝和炎症浸润。给予脑肠肽(5、10、20μg·kg-1) ip后可明显降低酒精性肝损伤小鼠增高的血清ALT、AST活性,改善酒精肝病理改变和炎症浸润;并能减少肝匀浆MDA含量,使降低的肝匀浆SOD活性升高;降低酒精性肝损伤小鼠肝脏的炎症细胞因子TNF-α、IL-1β、IFN-γ、IL-6和MCP-1的mRNA表达。结论脑肠肽对小鼠酒精性肝损伤具保护作用,其机制与抗氧化和抑制炎症作用有关。
目的:研究腦腸肽對小鼠酒精性肝損傷的保護作用。方法採用4週5%酒精飼料餵飼加5 g·kg-1的高劑量酒精灌胃誘導酒精性肝損傷模型,用分光光度法檢測血清中ALT、AST和肝勻漿MDA、SOD、GSH-Px含量;Real-time PCR法檢測肝髒中炎癥細胞因子 TNF-α、IL-1β、IFN-γ、IL-6和MCP-1的錶達。 HE染色檢測肝髒病理改變。結果這種慢性酒精餵飼+單劑量大劑量酒精灌胃模式可明顯誘導酒精性肝損傷,可導緻明顯的轉氨酶升高、脂肪肝和炎癥浸潤。給予腦腸肽(5、10、20μg·kg-1) ip後可明顯降低酒精性肝損傷小鼠增高的血清ALT、AST活性,改善酒精肝病理改變和炎癥浸潤;併能減少肝勻漿MDA含量,使降低的肝勻漿SOD活性升高;降低酒精性肝損傷小鼠肝髒的炎癥細胞因子TNF-α、IL-1β、IFN-γ、IL-6和MCP-1的mRNA錶達。結論腦腸肽對小鼠酒精性肝損傷具保護作用,其機製與抗氧化和抑製炎癥作用有關。
목적:연구뇌장태대소서주정성간손상적보호작용。방법채용4주5%주정사료위사가5 g·kg-1적고제량주정관위유도주정성간손상모형,용분광광도법검측혈청중ALT、AST화간균장MDA、SOD、GSH-Px함량;Real-time PCR법검측간장중염증세포인자 TNF-α、IL-1β、IFN-γ、IL-6화MCP-1적표체。 HE염색검측간장병리개변。결과저충만성주정위사+단제량대제량주정관위모식가명현유도주정성간손상,가도치명현적전안매승고、지방간화염증침윤。급여뇌장태(5、10、20μg·kg-1) ip후가명현강저주정성간손상소서증고적혈청ALT、AST활성,개선주정간병리개변화염증침윤;병능감소간균장MDA함량,사강저적간균장SOD활성승고;강저주정성간손상소서간장적염증세포인자TNF-α、IL-1β、IFN-γ、IL-6화MCP-1적mRNA표체。결론뇌장태대소서주정성간손상구보호작용,기궤제여항양화화억제염증작용유관。
Aim To investigate the effects of ghrelin on alcohol-induced liver injury. Methods The alcoholic liver injury mouse model was induced by chronic etha-nol feeding ( 4-week ad libitum oral feeding with the ethanol liquid diet) plus a single binge ethanol (5 g· kg-1 ) feeding. The level of alanine aminotransferase (ALT), aspartate aminotransferase (AST) in serum, malondiadehyde ( MDA ) content, superoxide dis-mutase (SOD) and glutathione peroxidase (GSH-Px) activities in liver homogenate were assayed by spectro-photometer. Hepatic pathological examination was ob-served by HE staining. The mRNA expression of proin-flammatory cytokines including TNF-α, IL-1β, IFN-γ, IL-6 and MCP-1 in the liver was measured by real-time PCR method. Results This chronic-plus-single-binge high dose ethanol feeding synergistically induced liver injury, inflammation and fatty liver change. Treatment with Ghrelin ( 5 , 10 , 20 μg · kg-1 ) significantly de-creased the enhanced level of transaminase ( ALT, AST) in serum, improved the pathologic change in liv-er, and reduced the infiltration of inflammatory cells induced by alcohol administration. Ghrelin also de-creased MDA content and increased the reduced SOD and GSH-Px level in liver homogenate. Furthermore, ghrelin decreased inflammatory cytokines mRNA ex-pression including TNF-α, IL-1β, IFN-γ, IL-6 and MCP-1 in the liver. Conclusion Ghrelin has protec-tive effects against alcoholic liver injury in mice via in-hibiting inflammation and suppressing oxidative stress.