CAJ | 학술논문

目的：观察糖肝康对糖尿病慢性肝损伤大鼠肝脏组织光镜病理结构、电镜超微结构和肝功能、细胞色素P450（ CYP450）的影响。方法将50只大鼠分为正常组、模型组、糖肝康小剂量组、糖肝康大剂量组、降糖甲组5组，每组10只。用链脲佐菌素和四氯化碳腹腔注射建立糖尿病慢性肝损伤大鼠模型。干预12周后，应用光镜和电镜观察各组大鼠肝脏病理结构和超微结构改变，比较各组大鼠肝功能，比较各组大鼠CYP4501A1，CYP4502E1，CYP4503A1指标。结果光镜下，模型组大鼠肝细胞大量脂肪变性、增生有异型性，可见核分裂象，肝小叶间有少量纤维组织增生；糖肝康大剂量组肝脏结构基本正常。电镜下，模型组大鼠肝细胞体积小，核变形、皱缩，有切迹，核仁明显，常染色质团块状，异染色质边聚，线粒体肿胀，亦可见线粒体空泡化，线粒体嵴模糊；内质网肿胀；可见大量脂滴。糖肝康大剂量组肝细胞结构基本正常。糖肝康小剂量组与模型组相比，ALT明显降低（P＜0．05）；糖肝康大剂量组与模型组相比，ALT明显降低（P＜0．01）；降糖甲组与模型组相比，ALT明显降低（P＜0．01）；糖肝康大剂量组与降糖甲组相比，ALT明显降低（P＜0．05）。糖肝康小剂量组与模型组相比，AST明显降低（ P＜0．01）；糖肝康大剂量组与模型组相比，AST明显降低（P＜0．01）；降糖甲组与模型组相比，AST明显降低（P＜0．05）；糖肝康大剂量组与降糖甲组相比，AST明显降低（P＜0．01）。糖肝康小剂量组、糖肝康大剂量组分别与模型组相比，CYP4501A1，CYP4502E1，CYP4503A1的表达均降低（P＜0．05）；降糖甲组与模型组相比，CYP4501A1， CYP4502E1，CYP4503A1的表达均降低（P＜0．05）；糖肝康大剂量组与降糖甲组相比，CYP4501A1，CYP4502E1，CYP4503A1的表达均明显降低（ P＜0．05）。结论糖肝康对肝脏的病理改变起到一定改善作用，还可以通过调节肝功能，CYP4501A1，CYP4502E1，CYP4503A1的表达，起到对肝脏的保护作用。目的：觀察糖肝康對糖尿病慢性肝損傷大鼠肝髒組織光鏡病理結構、電鏡超微結構和肝功能、細胞色素P450（ CYP450）的影響。方法將50隻大鼠分為正常組、模型組、糖肝康小劑量組、糖肝康大劑量組、降糖甲組5組，每組10隻。用鏈脲佐菌素和四氯化碳腹腔註射建立糖尿病慢性肝損傷大鼠模型。榦預12週後，應用光鏡和電鏡觀察各組大鼠肝髒病理結構和超微結構改變，比較各組大鼠肝功能，比較各組大鼠CYP4501A1，CYP4502E1，CYP4503A1指標。結果光鏡下，模型組大鼠肝細胞大量脂肪變性、增生有異型性，可見覈分裂象，肝小葉間有少量纖維組織增生；糖肝康大劑量組肝髒結構基本正常。電鏡下，模型組大鼠肝細胞體積小，覈變形、皺縮，有切跡，覈仁明顯，常染色質糰塊狀，異染色質邊聚，線粒體腫脹，亦可見線粒體空泡化，線粒體嵴模糊；內質網腫脹；可見大量脂滴。糖肝康大劑量組肝細胞結構基本正常。糖肝康小劑量組與模型組相比，ALT明顯降低（P＜0．05）；糖肝康大劑量組與模型組相比，ALT明顯降低（P＜0．01）；降糖甲組與模型組相比，ALT明顯降低（P＜0．01）；糖肝康大劑量組與降糖甲組相比，ALT明顯降低（P＜0．05）。糖肝康小劑量組與模型組相比，AST明顯降低（ P＜0．01）；糖肝康大劑量組與模型組相比，AST明顯降低（P＜0．01）；降糖甲組與模型組相比，AST明顯降低（P＜0．05）；糖肝康大劑量組與降糖甲組相比，AST明顯降低（P＜0．01）。糖肝康小劑量組、糖肝康大劑量組分彆與模型組相比，CYP4501A1，CYP4502E1，CYP4503A1的錶達均降低（P＜0．05）；降糖甲組與模型組相比，CYP4501A1， CYP4502E1，CYP4503A1的錶達均降低（P＜0．05）；糖肝康大劑量組與降糖甲組相比，CYP4501A1，CYP4502E1，CYP4503A1的錶達均明顯降低（ P＜0．05）。結論糖肝康對肝髒的病理改變起到一定改善作用，還可以通過調節肝功能，CYP4501A1，CYP4502E1，CYP4503A1的錶達，起到對肝髒的保護作用。
목적：관찰당간강대당뇨병만성간손상대서간장조직광경병리결구、전경초미결구화간공능、세포색소P450（ CYP450）적영향。방법장50지대서분위정상조、모형조、당간강소제량조、당간강대제량조、강당갑조5조，매조10지。용련뇨좌균소화사록화탄복강주사건립당뇨병만성간손상대서모형。간예12주후，응용광경화전경관찰각조대서간장병리결구화초미결구개변，비교각조대서간공능，비교각조대서CYP4501A1，CYP4502E1，CYP4503A1지표。결과광경하，모형조대서간세포대량지방변성、증생유이형성，가견핵분렬상，간소협간유소량섬유조직증생；당간강대제량조간장결구기본정상。전경하，모형조대서간세포체적소，핵변형、추축，유절적，핵인명현，상염색질단괴상，이염색질변취，선립체종창，역가견선립체공포화，선립체척모호；내질망종창；가견대량지적。당간강대제량조간세포결구기본정상。당간강소제량조여모형조상비，ALT명현강저（P＜0．05）；당간강대제량조여모형조상비，ALT명현강저（P＜0．01）；강당갑조여모형조상비，ALT명현강저（P＜0．01）；당간강대제량조여강당갑조상비，ALT명현강저（P＜0．05）。당간강소제량조여모형조상비，AST명현강저（ P＜0．01）；당간강대제량조여모형조상비，AST명현강저（P＜0．01）；강당갑조여모형조상비，AST명현강저（P＜0．05）；당간강대제량조여강당갑조상비，AST명현강저（P＜0．01）。당간강소제량조、당간강대제량조분별여모형조상비，CYP4501A1，CYP4502E1，CYP4503A1적표체균강저（P＜0．05）；강당갑조여모형조상비，CYP4501A1， CYP4502E1，CYP4503A1적표체균강저（P＜0．05）；당간강대제량조여강당갑조상비，CYP4501A1，CYP4502E1，CYP4503A1적표체균명현강저（ P＜0．05）。결론당간강대간장적병리개변기도일정개선작용，환가이통과조절간공능，CYP4501A1，CYP4502E1，CYP4503A1적표체，기도대간장적보호작용。
Objective To observe the effect of Tanggankang on pathogenic structure of liver with light microscope, ultra structure with electron microscopy, and hepatic function, CYP50 in diabetic liver inju-ry model rats.Methods 50 rats were randomly divided into control group, model group, low-dose of Tanggankang group,high-dose of Tanggankang group and first group of hypoglycemic, with 10 rats in each group.The diabetic liver injury model rats were established with intraperitoneal injection of streptozotocin ( STZ) and carbon tetrachloride.After treated for 12 weeks, light microscopy and electron microscopy were used to detect pathogenic structure and ultra structure in rats.The hepatic function CYP450 1A1, CYP450 2E1,CYP450 3A1 among groups were compared.Results Under light microscopy, lots of fatty degerenerations of hepatocyte happened in model group, and the hyperplasia showed atypia, as well as mitotic figure, between the hepatic lobule, a small amount of fiber texture showed proliferation.In high-dose of Tanggankang group, hepatic structure showed essentially normal.Under electron microscopy, small volume hepatocyte, nuclear showed distortion and shrinking, incisures could be seen in nuclear, nucleolus was obvious seen, euchromatin was crumby and heterochromatin was dispersive, mitochondria was swollen, vacuolation mitochondria could also be seen, mitochondrial cristae was obscure, swollen en-doplasmic reticulum and lipid droplet were seen.In high-dose of Tanggankang group, hepatocyte showed essentially normal.Compared to model group, alanine transaminase ( ALT) of low-dose of Tanggankang group decreased significantly ( P<0.05);compared to model group, ALT of high-dose of Tanggankang group decreased significantly ( P<0.01);compared to model group, ALT of first group of hypoglycemic decreased significantly (P<0.01), compared to first group of hypoglycemic, ALT of high-dose of Tang-gankang group decreased significantly ( P <0.05).Compared to model group, aspartate aminotrans-ferase ( AST) of low-dose of Tanggankang group decreased significantly ( P<0.01);compared to control group, AST of high-dose of Tanggankang group decreased significantly ( P<0.01); compared to model group, AST of first group of hypoglycemic decreased significantly ( P <0.05 ) , compared to the first group of hypoglycemic, AST of high-dose of Tanggankang group decreased significantly (P <0.01). compared to model group, the expressions of CYP450 1A1,CYP450 2E1,CYP450 3A1 showed signifi-cantly decrease in high and low dose of Tanggankang groups(P <0.05).The expressions of CYP450 1A1,CYP450 2E1,CYP450 3A1 of first group of hypoglycemic showed significantly decrease when com-paring with model group ( P <0 .05 ); compared to the first group of hypoglycemic, expressions of CYP450 1A1, CYP450 2E1, CYP450 3A1 showed significantly decrease in high-dose of Tanggankang group (P<0.05).Conclusions Tanggankang has certain improvement for pathological changes of the liver, and it can also protect the liver by regulating the expressions of CYP450 1A1,CYP450 2E1 and CYP450 3A1.