Effect of insulin and metformin on methylation and glycolipid metabolism of peroxisome proliferator-activated receptor γcoactivator-1A of rat offspring with gestational diabetes mellitus

Objective:To discuss the effect of insulin and metformin on amethylation and glycolipid metabolism of peroxisome proliferator-activated receptor γ coactivator-1A(PPARGC1A) of rat offspring with gestational diabetes mellitus(GDM).Methods:A total of 45 pregnant rats received the intraperitoneal injection of streptozotocin to establish the pregnant rat model of GDM.A total of 21 pregnant rats with GDM were randomly divided into three groups,with 7ruts in each group,namely the insulin group,metformin group and control group.Rats in the insulin group received the abdominal subcutaneous injection of 1 mL/kg recombinant insulin glargine at 18:00 every day.Rats in the metformin group received the intragastric infusion of metformin hydrochloride at 18:00 every day,with the first dose of 300 mg/kg.The doses of two groups were adjusted every 3 d to maintain the blood glucose level at 2.65-7.62 mmol/L.Rats in the control group received the intragastric infusion of 1 mL normal saline at 18:00 every day.After the natural delivery of pregnant rats.10 offspring rats were randomly selected from each group.At birth,4 wk and 8 wk after the birth of offspring rats,the weight of offspring rats was measured.The blood glucose level of offspring rats was measured at 4wk and 8 wk,while the level of serum insulin,triglyceride and leptin was measured at 8 wk.Results:The weight of offspring rats at birth in the insulin group and metformin group was significantly lower than the one in the control group(P0.05),and there was no significant difference at 4 wk and 8 wk among three groups(P0.05).The fasting blood glucose and random blood glucose in the insulin group and metformin group at 4 wk and 8 wk were all significantly lower than ones in the control group(P0.05);there was no significant difference between the insulin group and metformin group(P0.05).The expression of PPARGC1 A mRNA in the insulin group and metformin group was significantly higher and the methylation level of PPARGC1 A was significantly lower than the one in the control group(P0.05),but there was no significant difference between the insulin group and metformin group(P0.05).Insulin and leptin at 8 wk in the insulin group and metformin group were significantly higher,while triglyceride was significantly lower than the one in the control group(P0.05);triglyceride level of rats in the insulin group was significantly higher than the one in the metformin group(P0.05).There was no significant difference in insulin and leptin level of offspring rats between the insulin group and metformin group(P0.05).Conclusions:GDM can induce the methylation of PPARGC1 A of offspring rats to reduce the expression of PPARGC1 A mRNA and then cause the disorder of glycolipid metabolism when the offspring rats grow up;the insulin or metformin in the treatment of pregnant rats with GDM can reduce the methylation level of PPARGC1 A and thus improve the abnormal glycolipid metabolism of offspring rats.     

肝X受体表达与胰岛素抵抗肥胖大鼠的肝糖代谢相关

雄性SD大鼠27只分为对照组、肥胖组、肥胖伴糖尿病组.测定血皮质酮浓度,行正葡萄糖高胰岛素钳夹实验.采用实时PCR检测各组大鼠肝X受体(LXR)、11β-羟基类固醇脱氢酶l(11β-HSD1)和糖皮质激素受体(GR)mRNA的表达情况.肥胖组和肥胖伴糖尿病组大鼠较对照组具有明显的胰岛素抵抗.与对照组相比,肥胖组和肥胖伴糖尿病组肝LXR mRNA表达均显著升高,11β-HSD1 mRNA表达均显著降低(均P＜0.05).

Abstract：

Twenty-seven male SD rats were assigned to 3 groups: control, obese, and obese with diabetes groups. Serum corticosterone was determined and euglycemic-hyperinsulinemic clamp was carried out. Expressions of liver X receptor ( LXR), 11 β-hydroxysteroid dehydrogenase 1 ( 11 β-HSD1 ), and glucocorticoid receptor (GR) were determined by real-time PCR. Both groups of obese rats were insulin-resistant, with up-regulated LXR mRNA and down-regulated 11 β-HSD1 mRNA( both P＜0.05 ).     

Effects of glutamine supplementation on splenocyte cytokine mRNA expression in rats with septic peritonitis

AIM: To investigate the effects of glutamine (GLN)-enriched diets before and GLN-containing total parenteral nutrition (TPN) after sepsis or both on the secretion of cytokines and their mRNA expression levels in splenocytes of rats with septic peritonitis. METHODS: Rats were assigned to a control group and 4 experimental groups. The control group and experimental groups 1 and 2 were fed a semipurified diet, while experimental groups 3 and 4 had part of the casein replaced by GLN which provided 25% of the total nitrogen. After rats were fed with these diets for 10 d, sepsis was induced by cecal ligation and puncture (CLP), whereas the control group underwent a sham operation, at the same time, an internal jugular vein was cannulated. All rats were maintained on TPN for 3 d. The control group and experimental groups 1 and 3 were infused with conventional TPN, while the TPN in experimental groups 2 and 4 was supplemented with GLN, providing 25% of the total nitrogen in the TPN solution. All rats were kiued 3 d after sham operation or CLP to examine their splenocyte subpopulation distribution and cytokine expression levels. RESULTS: Most cytokines could not be detected in plasma except for IL-10. No difference in plasma IL-10 was observed among the 5 groups. The IL-2, IL-4, IL-10, and TNF-α mRNA expression levels in splenocytes were significantly higher in experimental groups 2 and 4 than in the control group and group 1. The mRNA expression of IFN-γ was significantly higher in the GLN-supplemented groups than in the control group and experimental group 1. The proportion of CD45Ra+ was increased, while those of CD3+ and CD4+ were decreased in experimental group 1 after CLP was performed. There were no differences in spleen CD3+ lymphocyte distributions between the control and GLN-supplemented groups. CONCLUSION: GLN supplementation can maintain T-lymphocyte populations in the spleen and significantly enhance the mRNA expression levels of Th1 and Th2 cytokines and TNF-αin the spleen of rats with septic peritonitis.     

己酮可可碱对非酒精性脂肪肝大鼠肝组织线粒体解耦联蛋白表达的影响

Objective To investigate the effects of pentoxifylline (PTX) on the expression of uncoupling protein 2 (UCP-2) of hepatic mitochondria in rats with nonalcoholic fatty liver disease (NAFLD). Methods Sixty SD rats were randomly divided into 3 groups (each n = 20): normal control group, experiment group and treatment group. The rats in normal control group were given a normal feed. The rats in experiment and treatment groups were given fat-rich feed. Furthermore, the rats in treatment group were given PTX after 4 weeks in fat-rich diet feeding. The expression of UCP-2 in the liver was detected by immunohistochemistry and semi-quantitative RT-PCR. Results The hepatic expression of UCP2 mRNA was higher in experiment group (4.0±0.3) than in normal control group (1.2±0.1). The hepatic expression of UCP2 mRNA was higher in treatment group (3.0±0.2) than in normal control group, but the hepatic expression of UCP2 mRNA was lower in treatment group than in experiment group (F = 160. 67, P＜ 0. 01). Conclusions The UCP-2 mRNA is expressed in livers of NAFLD, pentoxifylline plays an important role in the reduction of expression of UCP-2 mRNA in lives of NAFLD.     

Effects of emodin on treating murine nonalcoholic fatty liver induced by high caloric laboratory chaw

AIM: To investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by high caloric laboratory chaw. METHODS: Non-alcoholic fatty liver model was successfully established by feeding with high caloric laboratory chaw for 12 wk. Then the model rats were randomly divided into 3 groups, namely model control group, emodin group and dietary treatment group. The rats in emodin group were given emodin at dose of 40 mg/(kg·d) while animals in other groups were given distilled water of the same volume. The rats in model control group were fed with high caloric laboratory chaw while animals in other groups were fed with normal diet. Four weeks later, liver index (liver/body weight ratio), serum activities of liver-associated enzymes, blood lipid, fasting blood glucose, fasting plasma insulin, HOMA insulin resistance index (HOMA-IR), hepatic triglyceride content and histology features of all groups were assayed. The expression of hepatic peroxisomal proliferator activated receptor (PPAR) gamma was determined by RT-PCR. RESULTS: The body weight, liver index, serum activities of alanine aminotransferase (ALT), blood lipid, hepatic triglyceride content of model control group were significantly elevated, with moderate to severe hepatocyte steatosis. The expression of hepatic PPAR gamma mRNA was obviously reduced in model control group. Compared with model control group, the body weight, liver index, serum activities of ALT, blood lipids and hepatic triglyceride of emodin group significantly decreased and hepatic histology display was also greatly improved. Meanwhile, the expression of hepatic PPAR gamma mRNA was elevated. However, high serum activities of ALT and hyperlipidemia were persisted in dietary treatment group although liver index was decreased and liver histology was somewhat improved. CONCLUSION: It is suggested that emodin might be effective in the treatment of non-alcoholic fatty liver in rats. Its therapeutic mechanism could be associated with increasing the expression of hepatic PPAR gamma mRNA.     

Effects of arginine supplementation on splenocyte cytokine mRNA expression in rats with gut-derived sepsis

AIM: To investigate the effects of arginine (Arg)-enriched diets before sepsis and/or Arg-containing total parenteral nutrition (TPN) after sepsis or both on cytokine mRNA expression levels in splenocytes of rats with gut-derived sepsis. METHODS: Rats were assigned to four experimental groups. Groups 1 and 2 were fed with a semipurified diet, while groups 3 and 4 had part of the casein replaced by Arg which provided 2% of the total calories. After the rats were fed with these diets for 10 d, sepsis was induced by cecal ligation and puncture (CLP), at the same time an internal jugular vein was cannulated. All rats were maintained on TPN for 3 d. Groups 1 and 3 were infused with conventional TPN, while groups 2 and 4 were supplemented with Arg which provided 2% of the total calories in the TPN solution. All rats were killed 3 d after CLP to examine their splenocyte subpopulation distribution and cytokine expression levels. RESULTS: Plasma interleukin (IL)-2, IL-4, tumor necrosis factor-α(TNF-α) and interferon (IFN-γ) were not detectable 3 d after CLP. There were no differences in the distributions of CD45Ra+, CD3+, CD4+, and CD8+ cells in whole blood and splenocytes among the four groups. The splenocyte IL-2 mRNA expression in the Arg-supplemented groups was significantly higher than that in group 1. IL-4 mRNA expression in groups 3 and 4 was significantly higher than that in groups 1 and 2. The mRNA expression of IL-10 and IFN-γ was significantly higher in group 4 than in the other three groups. There was no difference in TNF-α mRNA expression among the four groups. CONCLUSION: The influence of Arg on the whole blood and splenic lymphocyte subpopulation distribution is not obvious. However, Arg administration, especially before and after CLP, significantly enhances the mRNA expression levels of Th1 and Th2 cytokines in the spleen of rats with gut-derived sepsis.     

Inhibition of Early Atherogenesis by Telemisartan and Rosiglitazone in Male Tats With Diabetes Mellitus

Objectives To observe the effects of telmisartan and rosiglitazone and explore the mechanism on early atherogenesis in male rats with type 2 diabetes mellitus. Methods Forty male SD rats were randomly and equally divided into four groups： control group, type 2 diabetes mellitus group, telmisartan group and rosiglitazone group. High lipid and high glucose were used for inducing DM in SD rats. The rats were raised for sixteen weeks. TC, TG, LDL-C and BG, PGI were measured. The aortae were collected for histopathlogical and immunohistochemical studies. Immunohisto-chemistry was used to analyze the expression of PPAR-γ, VCAM-1 and ICAM-1 in the arterial vessel wall. Results Compared with the control group, the level of TC, TG, LDL-C, and BG in blood were increased significantly （P 〈 0. 01 ） in type 2 Diabetic group. The telmisartan and rosiglitazone treatment decreased blood TC, TG, LDL-C and BG. The expression of PPAR-γ in type 2 diabetic group, telmisartan and rosiglitazone groups had significant differences compared with the control group, but there wasn＇t any significant differences （ P 〉 0. 05 ） among those three groups. Expression of VCAM-1, ICAM-1 and the monocytes infilitrating into the intima of the aortas telmisartan and rosiglitazone group was significantly lower than those in diabetic group （P 〈 0.01 ）. The endothelial damage of the aortae in telmisartan and rosiglitazone group was less severe than that in diabetes mellitus group. Conclusion Telmisartan and rosiglitazone can prevent early atherogenesis through alleviating the damage to the arterial wall by increasing the activation of PPAR-γ and inhibiting the VCAM-1, ICAM-1 expression and the monocytes infilitrating into the arterial wall. （S Chin J Cardio12009 ; 10（4） ： 216 -221 ）     

Effect of endogenous insulin-like growth factor and stem cell factor on diabetic colonic dysmotility

AIM: To investigate whether the reduction of stem cell factor (SCF) is mediated by decreased endogenous insulin-like growth factor (IGF)-1 in diabetic rat colon smooth muscle. METHODS: Sixteen Sprague-Dawley rats were randomly divided into two groups: control group and streptozotocin-induced diabetic group. After 8 wk of streptozotocin administration, colonic motility function and contractility of circular muscle strips were measured. The expression of endogenous IGF-1 and SCF was tested in colonic tissues. Colonic smooth muscle cells were cultured from normal adult rats. IGF-1 siRNA transfection was used to investigate whether SCF expression was affected by endogenous IGF-1 expression in smooth muscle cells, and IGF-1 induced SCF expression effects were studied. The effect of high glucose on the expression of endogenous IGF-1 and SCF was also investigated. RESULTS: Diabetic rats showed prolonged colonic transit time (252 ± 16 min vs 168 ± 9 min, P < 0.01) and weakness of circular muscle contraction (0.81 ± 0.09 g vs 2.48 ± 0.23 g, P < 0.01) compared with the control group. Endogenous IGF-1 and SCF protein expression was significantly reduced in the diabetic colonic muscle tissues. IGF-1 and SCF mRNA expression also showed a paralleled reduction in diabetic rats. In the IGF-1 siRNA transfected smooth muscle cells, SCF mRNA and protein expression was significantly decreased. IGF-1 could induce SCF expression in a concentration and time-dependent manner, mainly through the extracellular-signal-regulated kinase 1/2 signal pathway. High glucose inhibited endogenous IGF-1 and SCF expression and the addition of IGF-1 to the medium reversed the SCF expression. CONCLUSION: Myopathy may resolve in colonic motility dysfunction in diabetic rats. Deficiency of endogenous IGF-1 in colonic smooth muscle cells leads to reduction of SCF expression.     

高糖对肾小管上皮细胞ACE/ACE2表达的影响

体外培养的HK-2细胞分为正常对照组(NG组)、高糖组(HG组)、渗透压对照组(MG组),检测细胞ACE、ACE2 mRNA和蛋白表达及细胞上清液血管紧张素Ⅱ的浓度.结果 在NG组,正常培养的HK-2细胞即存在ACE、ACE2 mRNA及蛋白表达.在HG组HK-2细胞,ACE mRNA及蛋白表达较NG组升高,而ACE2mRNA及蛋白表达降低.在HG组血管紧张素Ⅱ水平较NG组显著升高.结果 表明高糖可促进体外培养的HK-2细胞ACE表达、抑制ACE2表达,进而促进血管紧张素Ⅱ合成.

Abstract：

HK-2 cells cultured in vitro were divided into three groups: normal glucose group ( NG ), high glucose group( HG), and mannitol group(MG). The expression of angiotensin-converting enzyme( ACE ) and ACE2 mRNA in HK-2 cells was detected. The concentration of angiotensin Ⅱ ( Ang Ⅱ ) in the culture medium was detected. The mRNA and protein expression of ACE and ACE2 existed in normal cultured HK-2 ( NG group ). In comparison with NG group, the mRNA and protein expressions of ACE in HG group increased significantly ( P＜0. 01 ), and the expression of ACE2 mRNA decreased significantly( P＜0. 01 ). The level of Ang Ⅱ in HG group was significantly higher than in NG group( P＜0. 05 ). The result show that high glucose may induce ACE expression and inhibit ACE2 expression, then promote synthesis of Ang Ⅱ in proximal tubular cells.     

Eugenosedin-A improves glucose metabolism and inhibits MAPKs expression in streptozotocin/nicotinamide-induced diabetic rats

This study examined the effects of eugenosedin-A (Eu-A) in a streptozotocin (STZ)/nicotinamide-induced rat model of type II diabetes mellitus (T2DM). Six-week-old Sprague–Dawley rats were randomly divided into three groups: (1) RD group, normal rats fed a regular diet (RD), (2) DM group, T2DM rats fed a high-fat diet, and (3) Eu-A group, T2DM rats fed a high fat diet plus oral Eu-A (5 mg/kg/day). After 30 days, the DM group had higher body weight, higher blood glucose and lower insulin levels than the RD group. The DM group also had increased protein expression of glycogen synthase kinase (GSK) in liver and skeletal muscle and decreased protein expression of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), IRS-2, AMP-activated protein kinase (AMPK), glucose transporter-4 (GLUT-4), glucokinase (GCK), and peroxisome proliferator-activated receptor γ (PPAR-γ). STZ/nicotinamide-induced T2DM increased the expression of mitogen-activated protein kinases (MAPKs: p38, ERK, JNK) and inflammatory p65 protein. In the Eu-A treated T2DM rats, however, blood glucose was attenuated and the insulin concentration stimulated. Changes in IR, IRS-1 and IRS-2 proteins as well as AMPK, GLUT-4, GCK, GSK, PPAR-γ, MAPKs, and inflammatory p65 proteins were ameliorated. These results suggested that Eu-A alleviates STZ/nicotinamide-induced hyperglycemia by improving insulin levels and glucose metabolism, and inhibiting the MAPKs- and p65-mediated inflammatory pathway.     

葡萄糖激酶mRNA、葡萄糖转运蛋白2在慢性乙型重型肝炎患者糖代谢异常中的作用

目的通过研究葡萄糖激酶（GCK）mRNA、葡萄糖转运蛋白2（GLUT2）在慢性乙型重型肝炎（慢重肝）患者肝组织中的表达来初步探讨其在慢重肝糖代谢异常中的作用。方法运用RT-PCR法测定10例慢重肝患者和10例肝硬化（CTP评分A级）患者肝脏GCK mRNA的表达;免疫组织化学方法检测上述10例慢重肝患者及10例正常对照肝组织GLUT2表达。两组间均数比较采用t检验,相关性采用Pearson相关分析。结果慢重肝肝组织GCK mRNA表达低于肝硬化组,（1.13±0.11）vs（1.44±0.14）,P〈0.05。慢重肝肝组织GCK mRNA水平与碳水化合物氧化率呈正相关（r=0.845,P〈0.01）,与空腹血糖无明显相关性（r=0.03,P〉0.05）。慢重肝肝组织GLUT2表达减少,且分布在假小叶结节周围细胞。结论肝脏GCK mRNA水平与糖氧化利用密切相关,GCK mRNA与GLUT2表达减少是慢重肝糖代谢障碍发生的机制之一。     

糖尿病大鼠肝X受体、11β-羟基类固醇脱氢酶和糖皮质激素受体表达的改变

目的:探讨肝X受体(LXR)、11β-羟基类固醇脱氢酶1(11β-HSD1)和糖皮质激素受体(GR)在糖尿病发生、发展中的作用和意义。方法:应用链佐脲菌素(STZ)诱导建立糖尿病大鼠模型,将正常大鼠作为对照组。应用实时定量-聚合酶链反应(real-time PCR)的方法测定2组大鼠肝组织内LXR mRNA、11β-HSD1 mRNA和GR mRNA的表达。结果:糖尿病组大鼠肝组织内LXR mRNA较对照组明显升高(P     

2型糖尿病胃促生长素受体的表达与胃排空关系

目的 探讨2型糖尿病大鼠下丘脑和胃组织中胃促生长素(ghrelin)受体(GHSR)表达变化与胃排空的关系.方法 将大鼠分为糖尿病组、单纯肥胖组和对照组.糖尿病组和单纯肥胖组大鼠给予高糖和高脂饮食,糖尿病组8周后注射小剂量链脲佐菌素(STZ).检测各组大鼠体重、空腹血糖和胰岛素水平,并计算胰岛素抵抗指数.酚红灌胃法检测胃排空,实时定量荧光RT-PCR测定下丘脑和胃组织中GHSR mRNA表达.结果 糖尿病组和单纯肥胖组饲养8周后,体重和胰岛素水平较对照组明显升高(P＜0.01),血糖较对照组增高,但差异无统计学意义(P＞0.05).注射STZ后,糖尿病组胰岛素水平显著下降,血糖水平明显升高(P＜0.05).糖尿病组和单纯肥胖组液体胃排空低于对照组(P＜0.05),下丘脑和胃组织GHSR mRNA表达均明显下降(P＜0.05),并与胃排空下降呈正相关(P＜0.05).结论 2型糖尿病大鼠下丘脑和胃组织中GHSR mRNA的表达下降,降低了胃促生长素的促胃肠动力作用,从而有可能参与了糖尿病胃排空的延迟.可能与糖尿病胃排空障碍有关.     

肝脏胰岛素抵抗与肝糖输出调控基因表达的关系

目的观察高脂饮食饲养造成的肝脏胰岛素抵抗与肝糖输出有关的调控基因表达的关系。方法将8周龄雄性SD大鼠随机分为2组:正常饲养组(10例)和高脂饮食饲养组(10例)。饲养期间动态观察体重和空腹血糖变化趋势。饲养至28周实验终点时取空腹血测胰岛素和甘油三酯。采用肝脏对3H-2- 脱氧葡萄糖的摄取能力测定各组的肝脏胰岛素敏感性,用蒽酮法测定肝糖原含量,并用逆转录聚合酶链反应法分析糖异生和糖原合成关键酶肝脏磷酸烯丙醇羧激酶、葡萄糖-6-磷酸酶、糖原合成酶和PPAR γ协同刺激因子1 α的mRNA表达的变化。结果高脂饮食饲养大鼠出现明显腹型肥胖。血浆甘油三酯水平升高。饲养18周开始,高脂饮食组空腹血糖增加[正常饲养组(4．77±0．63)mmol／L,高脂饮食组[(5．45± 0.87)mmol／L,P<0．05],此差异持续到28周;肝脏3H-2-脱氧葡萄糖摄取率高脂饮食组较正常饲养组下降42．0％,肝糖原含量增加92．4％(P<0．01)l磷酸烯丙醇羧激酶mRNA增加41．5％,协同刺激因子1α mRNA增加30．8％(P<0．05)。结论长期高脂饮食诱导肝脏协同刺激因子1α和肝脏磷酸烯丙醇羧激酶基因表达,糖异生增加,同时肝糖分解不能相应受到抑制,导致肝糖输出增加及空腹血糖升高。     

间歇低氧大鼠肝细胞GLUT-2、GCK表达与胰岛素抵抗的相关性研究

目的 检测葡萄糖转运蛋白-2(GLUT-2)、葡萄糖激酶(GCK)在间歇低氧大鼠模型肝细胞中表达的变化,探讨间歇低氧引起胰岛素抵抗的相关机制.方法 24只6周龄健康雄性SpragueDawley(SD)大鼠按照随机数字表法分为对照组、间歇低氧4周组(IH4组)和间歇低氧8周组(IH8组),每组8只.间歇低氧组按预设通气模式每天给予间歇低氧暴露8h,对照组给予间歇压缩空气,暴露时间同IH4组.实验结束后测定各组大鼠空腹血糖、空腹胰岛素,计算稳态模型评估-胰岛素抵抗指数(HOMA-IR)及胰岛素敏感性指数(ISI).免疫组织化学染色观察肝细胞GLUT-2、GCK蛋白表达变化,并利用平均灰度值对蛋白进行定量分析.结果 与对照组相比,IH4组及IH8组空腹血糖、空腹胰岛素、HOMA-IR均升高,ISI均降低,且IH8组更明显(F=161.92、51.46、126.99、83.87,P均＜0.05).与对照组相比,IH4组及I-H8组肝细胞GLUT-2、GCK蛋白表达均降低,且IH8组更显著(F=184.91、240.85,P均＜0.05).Pearson相关分析显示,GLUT-2、GCK平均灰度值与ISI呈负相关(r=-0.886、-0.906,P均＜0.05),与HOMA-tR呈正相关(r=0.894、0.869,P均＜0.05).结论 间歇低氧暴露使大鼠肝细胞GLUT-2、GCK蛋白表达下调,可能参与间歇低氧条件下胰岛素抵抗的发生.     

中药含药血清对高糖诱导心肌细胞促炎因子巨噬细胞移动抑制因子表达的影响简

目的 探讨益气化痰清毒方煎剂对巨噬细胞移动抑制因子（macrophage migration inhibitory factor,MIF）水平的影响及其含药血清对高糖诱导心肌细胞株（H9C2） MIF表达的影响.方法 制备中药煎剂（药物为黄芪、党参、毛冬青等）,取40只SD大鼠随机（随机数字表法）分4组（空白对照组、低、中、高剂量组）,完成灌药后用酶联免疫吸附试验（ELISA）法测各组动物血清MIF浓度;制备各组含药血清,分别干预经33 mmol/L葡萄糖处理后的H9C2心肌细胞,用反转录聚合酶链反应（RT-PCR）法测定各组细胞MIF mRNA的表达.结果 与对照组相比,经低、中、高剂量药物干预的大鼠血清MIF浓度均呈减少趋势,差异有统计学意义（P＜0.05）.经高糖处理的H9C2细胞MIF表达明显增加,在含药血清干预后MIF表达明显减少,且各组含药血清对MIF表达均有明显抑制作用,差异均有统计学意义（P＜0.05）,其中高剂量组效果最显著（P＜0.01）.随着药物浓度的增加,MIF表达呈减少趋势.结论 益气化痰清毒方可降低大鼠血清MIF浓度,其含药血清对高糖诱导H9C2心肌细胞MIF表达有明显抑制作用.