绿麦隆复合体系对小鼠睾丸组织的影响

目的：研究绿麦隆复合体系对小鼠睾丸组织的影响。方法：雄性昆明小鼠经口染毒绿麦隆25d，取睾丸组织作为标本观察。结果：绿麦隆单体系及复合体系各剂量组对小鼠睾丸均有不同程度的改变。光镜观察所见：生精上皮细胞排列疏松、紊乱；生精细胞脱落，层次减少。电镜观察所见：生精细胞线粒体呈空泡样改变，核膜肿胀、弯曲，支持细胞数目减少，部分细胞紧密连接破坏。结论：小鼠睾丸呈细胞退行性改变趋势，随剂量增加及复合染毒，病变加重。     

3种方式染毒丙烯酰胺对雄性小鼠早期精细胞微核的影响

目的研究腹腔注射、灌胃、皮肤染毒丙烯酰胺(AA)对小鼠早期精细胞微核发生率的影响,以反映相应的遗传毒性。方法将24只清洁级健康雄性昆明小鼠随机分为4组,分别为空白对照组、腹腔注射染毒组、灌胃染毒组和皮肤染毒组,每组6只。染毒剂量为25 mg/kg,每天1次,连续染毒5 d。首次染毒后第19天称体重和睾丸重量,计算睾丸系数。采用早期精细胞微核实验测定各组小鼠早期精细胞微核的发生率。结果染毒后腹腔注射染毒组、灌胃染毒组和皮肤染毒组小鼠体重均低于空白对照组,差异有统计学意义(P<0.05或P<0.01);与空白对照组比较,腹腔注射染毒组、灌胃染毒组和皮肤染毒组小鼠的睾丸重量均较低,差异有统计学意义(P<0.05);与空白对照组比较,腹腔注射染毒组和皮肤染毒组小鼠早期精细胞微核发生率较高,但差异无统计学意义(P>0.05),灌胃染毒组小鼠早期精细胞微核发生率高,差异有统计学意义(P<0.05)。结论 AA可致雄性小鼠早期精细胞微核发生率增高,且以灌胃染毒方式产生的毒性作用最为敏感。     

奥硝唑对大鼠睾丸和附睾超微结构的影响

目的 考察奥硝唑(ORN)对雄性大鼠睾丸、附睾超微结构的影响.方法 选取健康成年雄鼠40只,随机分成正常组(1%CMC-Na溶液)、ORN低、中、高剂量组(100、400和800 mg·kg-1·d-1),连续灌胃给药20 d.于末次给药24 h后取材,常规电镜制片,透射电镜观察各组睾丸、附睾超微结构.结果 电镜观察显示:(1)低剂量组睾丸、附睾超微结构与正常对照组无明显差异;(2)中剂量组附睾主细胞内可见空泡;睾丸少数生精小管层次紊乱,线立体肿胀、嵴模糊,胞质中其它细胞器偶见肿胀、溶解、空泡化现象;(3)高剂量组附睾管壁主细胞含空泡,纤毛排列紊乱,附睾管腔可见大量异型精子及坏死细胞残留物.睾丸牛精小管细胞胞质含有大量空泡;变态完成的精子数目很少;生精管腔填满了坏死脱落的各种细胞;部分精子顶体膜破裂,尾部轴丝包膜水肿起皱.结论 奥硝唑中、高剂量能引起附睾、睾丸发生超微病理改变.病理改变的部位和程度与剂量相关.     

邻苯二甲酸二乙基己酯与双酚A混合染毒对大鼠睾丸损伤及与氧化应激关系研究

目的研究邻苯二甲酸二乙基己酯(DEHP)和双酚A(BPA)混合染毒对大鼠睾丸损伤作用及与氧化应激关系。方法将32只4周龄SD大鼠随机分为750 mg/kg·bw DEHP、100 mg/kg·bw BPA、750 mg/kg·bw DEHP+100 mg/kg·bw BPA和溶剂对照组,每组8只;用玉米油配制成相应浓度,以5 ml/kg·bw容积连续灌胃染毒6周,1次/d。观察大鼠睾丸脏器系数和组织病理改变、精子数目、血清睾酮(T)和雌二醇(E2)含量,检测睾丸组织丙二醛(MDA)、过氧化氢(H2O2)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)水平,以及氧化应激相关因子SOD、GSH-Px、核因子E2相关因子2(Nrf2)、血红素加氧合酶(HO-1)、γ-谷氨酸半胱氨酸合成酶(Gclc)和硫氧还蛋白还原酶(Txnrd)的基因表达。结果 DEHP组及混合剂量组睾丸脏器系数及3个剂量组精子数目明显低于对照组(P0.05),光学显微镜下可见曲细精管萎缩、生殖细胞大部分消失;混合剂量组血清T水平显著低于对照组(P0.05);混合剂量组MDA含量升高、SOD活性下降,DEHP组MDA含量和GSH-Px活性均升高,BPA组SOD活性降低,差异均具有统计学意义(P0.05);混合染毒组的SOD1基因表达降低、SOD3和GSH-Px升高,差异具有统计学意义(P0.05);混合染毒组Gclc、Txnrd和Nrf2表达低于对照组,DEHP组Txnrd表达也降低,而BPA组Txnrd、Nrf2表达均升高,差异均有统计学意义(P0.05)。结论 DEHP和BPA单独及混合染毒均能导致大鼠睾丸发育不良,生精细胞减少,精子总数下降;可诱导睾丸产生氧化应激,破坏体内抗氧化稳态失衡;DEHP和BPA混合染毒可导致更严重损害。     

二乙氧基乙醇对大鼠睾丸生精细胞中Bax、细胞色素C和Caspase-3表达的影响

目的研究二乙氧基乙醇(2-Ethoxyethanol,2-EE)对大鼠睾丸生精细胞中Bax,细胞色素C(Cytochrome C,CytC)以及Caspase-3表达的影响,探讨其在生精细胞凋亡调控中的作用。方法选择Wistar大鼠,分别给予剂量400、800和1200mg/kg的2-EE,连续灌胃7d,对照组以等量生理盐水灌胃,分别于末次染毒后第1和29天处死动物。采用免疫组化法(SP法),观察不同剂量染毒后及自然恢复4周后生精细胞中Bax,CytC以及Caspase-3的表达情况。结果400、800和1200mg/kg染毒7d后,大鼠睾丸生精细胞中Bax,CytC以及Caspase-3的表达水平不同程度的上升,尤其以800mg/kg组最为明显。自然恢复4周后,生精细胞中Bax,CytC以及Caspase-3的表达基本接近对照组水平。结论在本试验条件下,2-EE急性染毒可能通过影响大鼠睾丸生精细胞中Bax,CytC和Caspase-3的释放,调控生精细胞凋亡,与2-EE所致睾丸毒性的可恢复性高度相关。     

三硝基甲苯对小鼠睾丸和卵巢形态学影响的研究

本文报告TNT对小鼠睾丸、卵巢形态学影响研究结果。选体重18～25克雄、雌小鼠各55只,随机分五组,实验组分高、中、低三组和阴性、阳性对照组。TNT染毒小鼠睾丸,光镜下主要改变是各级生精细胞减少。电镜下高、中剂量组见生精细胞明显损伤,如细胞核固缩、溶解、线粒体局灶性     

龙葵碱对小鼠睾丸支持细胞波形蛋白表达的影响

目的探讨龙葵碱对小鼠睾丸支持细胞波形蛋白表达的影响。方法将40只雄性昆明小鼠随机分为4组,A组腹腔注射等剂量0.9%NaCl,B、C、D组分别腹腔注射龙葵碱5、10和20 mg/kg,连续染毒14 d,取出睾丸组织。利用苏木素-伊红(HE)染色、睾丸重量、脏器系数的改变观察小鼠睾丸的病理学变化;利用免疫组织化学法检测睾丸波形蛋白的表达和变化。结果 实验表明,与对照组相比,20 mg/kg组的小鼠睾丸组织切片病理变化明显,曲细精管明显萎缩,大量细胞脱落至管腔及管腔外面,生精细胞与支持细胞分离,管腔内细胞排列紊乱,精子生成数大量减少;10和20mg/kg组的小鼠睾丸脏器系数(0.346±0.020、0.222±0.050)明显低于对照组(0.416±0.065),结果具有统计学意义(P0.05);20 mg/kg组小鼠睾丸波形蛋白表达明显下降,排列无序,阳性支持细胞脱落至曲细精管官腔之中。结论在本试验条件下,龙葵碱可能通过影响支持细胞波形蛋白的表达产生雄性生殖毒性。     

醋酸铅染毒小鼠睾丸和附睾组织病理学观察

成年小鼠经口给予醋酸铅500、100O、2000(mg·kg)/d连续28天。光镜观察发现:睾丸生精小管萎缩,生精细胞脱落、变性,层次减少、核固缩,随醋酸铅剂量增加,睾丸生精上皮病变加重;附睾管内出现大量精子细胞和精母细胞。电镜观察发现;1000mg/kg组小鼠睾丸精子细胞核变形,核染色质异常聚集;附睾精子轴丝变性浓缩,残余胞质增多,残余胞质内出现多个溶酶体,精子头核染色质成团块状,核液化,顶体破坏。     

乙体氯氰菊酯对雄性大鼠睾丸的损伤作用

目的　探讨乙体氯氰菊酯 (β CP)对雄性大鼠的睾丸毒性。 方法　成年Wistar雄性大鼠 ,分别以 0、2 0、40和80mg kg剂量的 β CP连续 8周灌胃染毒 ,按常规方法对染毒大鼠进行精子数、精子活动度和精子畸形检测 ,并对睾丸进行组织病理学检查。结果　 80mg kg剂量组大鼠活精率 (60 5 % )及精子活动度 (56 55 % )明显低于对照组 (分别为78 75 %和 72 2 0 % ) ,差异有显著性 (P <0 0 5) ,睾丸支持细胞和各级生精细胞发生病理改变。 2 0和 40mg kg剂量组均未见异常。结论　高剂量的 β CP对雄性大鼠睾丸有损伤作用     

慢性海洛因中毒致大鼠睾丸、附睾及精囊组织病理学改变

利用光镜及电镜对大白鼠慢性海洛因中毒模型及对照组的睾丸、附睾及精囊作组织细胞形态学检查。光镜结果表明，海洛因中毒组大鼠睾丸生精管生精上皮细胞层次明显减少，腔内精子稀少，畸形精子及脱落的生精细胞增多；附睾及精囊均存在腔内精子明显减少。电镜结果表明，海洛因中毒组大鼠睾九精子细胞减少，部分精子细胞变性、脱落，精子提前成熟，精子颈段线粒体肿胀，精子减少；支持细胞水肿，个别支持细胞核内水肿，支持细胞内溶酶体明显增多；精原细胞出现核膜扩张；精母细胞停滞于分裂前期；个别问质细胞破坏。附睾管上皮主细胞内溶酶体及吞噬泡明显增多，腔内精子减少，有较多的膜样小体，主细胞静纤毛局部明显减少。研究结果从组织病理学角度，证实了慢性海洛因中毒可导致睾丸生精功能明显障碍。     

中药复方脑还丹对快速老化鼠SAM-P/8海马CA1区超微结构的影响

目的探讨中药复方脑还丹对快速老化鼠海马CAl区超微结构的影响。方法3月龄雄性SAM/P 8小鼠30只,随机分成对照组、脑还丹低剂量组、脑还丹高剂量组,分别给予生理盐水及不同剂量中药复方脑还丹灌胃治疗4月,取海马制作电镜标本,透射电镜观察海马CAl区神经元超微结构。结果对照组脂褐素增多,溶酶体数目增多且空化,粗面内质网偶有扩张或膜结构断裂,核糖体数目明显减少,线粒体数目减少,线粒体肿胀、核膜增厚,嵴断裂或萎缩成中空状,细胞核核膜模糊, 核周池不清,染色质呈凝聚样改变,核周空泡明显。脑还丹组上述变化明显减轻。结论脑还丹能够减轻神经元退行性变化。     

Oxidative DNA damage induced by di-(2-ethylhexyl) phthalate in HEK-293 cell line

Di-(2-ethylhexyl) phthalate (DEHP) is commonly employed as a plasticizer. We have found that exposure of human embryonic kidney cell line 293 (HEK-293) to DEHP resulted in a crucial dose-dependent increase of DNA strand breaks in a comet assay. To elucidate the role of glutathione (GSH) in the DNA damage, the cells were pretreated with buthionine-(S,R)-sulfoximine (BSO) and pretreated with N-acetylcysteine (NAC), a GSH precursor. Here we show that depletion of GSH in HEK-293 cells with BSO dramatically increased the susceptibility of HEK-293 cells to DEHP-induced DNA damage. Furthermore, when the intracellular GSH content was elevated by NAC, the DNA damage induced by DEHP was almost completely abolished. In addition, DEHP had effect on lysosomal or mitochondrial damage at high dose level. These results indicate that DEHP exerts genotoxic effects in HEK-293 cells, probably through DNA damage induced by oxidative stress; GSH is responsible for cellular defense against DEHP-induced DNA damage; lysosome and mitochondria may be the vital targets in DEHP-induced DNA damage.     

乙醇诱导大鼠肝脏超微结构改变与护肝灵的干预

目的 观察护肝灵对乙醇诱导的大鼠肝脏超微结构改变的影响.方法 以乙醇灌胃法诱导大鼠肝损伤模型,护肝灵高、低剂量干预,易善复为阳性对照,连续42 d,H-600Ⅳ型透视电镜观察肝细胞超微结构和糖原.结果 乙醇灌胃各组大鼠的肝细胞出现不同程度的核固缩、线粒体肿胀、内质网扩张,偶见酒精小体(Mallory小体);细胞内出现脂滴;细胞间出现胶原纤维;糖原减少或消失.护肝灵低剂量组与阳性药相当,肝细胞核轻微固缩;线粒体肿胀明显,嵴断裂消失,粗面内质网扩张;偶见糖原.高剂量组肝细胞超微结构清晰,优于阳性药,与阴性对照组比较无显著差异.结论 护肝灵对乙醇诱导的大鼠肝细胞超微结构破坏有保护作用.     

Vitamin E protection from testicular damage caused by intraperitoneal aluminium

Different forms of Aluminium (Al) are environmental xenobiotics that induce free radical-mediated cytotoxicity and reproductive toxicity. Vitamin E (alpha -tocopherol) is an antioxidative agent that has been reported to be important for detoxification pathways. This study was thus aimed at elucidating the protective effects of vitamin E towards aluminium toxicity on the histology of the rat testis. Al (5 mg/kg body weight) was administered intraperitoneally in 2 ml saline, either alone or immediately before vitamin E (500 mg/kg body weight), at a different point of abdomen, and the alterations in the testis tissue were analyzed histologically. Seven treated animals were sacrificed for each group, with the testes removed and examined histologically. In the Al-treated group, the germinal epithelium of the seminiferous tubules was thinner in places and spermatids were almost absent; sperm numbers were low and there were no sperm in the lumen. In the Al plus vitamin E rats, there were large numbers of spermatids and sperm in the seminiferous tubule lumen. In the vitamin E alone group, a normal histology was seen. Electron microscopically, in the Al-treated group there were irregularities in the nuclear membrane, some damaged mitochondria, a decrease in the number of ribosomes, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. In the Al plus vitamin E group, the spermatogeneic cells and the sertoli cell cytoplasm showed an almost normal appearance. The ultrastructure of the testis in the vitamin E alone group showed a normal appearance. In conclusion, vitamin E antagonizes the toxic effects of Al at the histological level, thus potentially contributing to an amelioration of the testis histology in the Al-treated rats. The associated biochemical parameters merit further investigation.     

Toxicity of di(2-ethylhexyl)phthalate (DEHP) and di(2-ethylhexyl)adipate (DEHA) under conditions of renal dysfunction induced with folic acid in rats: enhancement of male reproductive toxicity of DEHP is associated with an increase of the mono-derivative

F344 male rats were given five consecutive weekly subcutaneous injections of folic acid for induction of chronic renal dysfunction and then di(2-ethylhexyl)phthalate (DEHP) or di(2-ethylhexyl)adipate (DEHA) in the diet at a concentration of 0, 6000 or 25,000 ppm for 4 weeks in order to investigate whether male reproductive toxicity of the two chemicals might be enhanced under conditions of renal disease. Control animals also received DEHP or DEHA in the same manner but without folic acid pretreatment. Decreased testicular weights, seminiferous atrophy with vacuolization of sertoli cells and diminished sperm counts were more prominent in rats given folic acid and then 25,000 ppm DEHP as compared to those exposed to DEHP alone. No such reproductive toxicity was evident in rats given 6000 ppm DEHP or either dose of DEHA. An increased concentration of the mono-derivative of DEHP (mono(2-ethylhexyl)phthalate, MEHP) in the blood, testis and urine was considered relevant to the enhanced reproductive toxicity observed with DEHP.     

The absorption, metabolism and tissue distribution of di(2-ethylhexyl)phthalate in rats

Rats given a single oral dose of [¹⁴C] di(2-ethylhexyl) phthalate [¹⁴C] (DEHP) excreted 42% and 57% of the dose in the urine and faeces respectively in 7 days. A significant proportion (14%) of the dose is excreted in bile. Rats fed 1000 ppm DEHP in the diet for 7 days prior to dosing with [¹⁴C] DEHP excreted 57% and 38% in the urine and faeces respectively in 4 days.When fed continuously to rats at dietary concentrations of 1000 and 5000 ppm, the amount of the ester in liver and abdominal fat rapidly attains a steady-state concentration and there is no evidence of accumulation. When returned to a normal diet, the radioactivity in the liver declined with a half life of 1–2 days while that in fat declined rather more slowly to give a half life of 3–5 days. The relative liver weight increased to a level 50% above normal in rats receiving 5000 ppm DEHP and returned to normal within 1 week after being returned to normal diet.When administered intravenously DEHP is preferentially localised in lung, liver and spleen from where it is eliminated with a half-life of 1–2 days.The hexobarbital sleeping time was reduced by 30–40% in rats following repeated oral administration of DEHP; when the ester was administered intravenously sleeping time was increased by approx. 40%.DEHP is extensively metabolised after oral administration, the principal metabolites being identified as the acid, alcohol and ketone resulting from ω- and (ω-1)-oxidation of mono(2-ethylhexyl) phthalate (MEHP). DEHP is rapidly hydrolysed to the half-ester by pancreatic lipase.     

The adverse effects of low‐dose exposure to Di(2‐ethylhexyl) phthalate during adolescence on sperm function in adult rats

Di(2‐ethylhexyl) phthalate (DEHP) is the most crucial phthalate derivative added to polyvinyl chloride as a plasticizer. This study examined the effects of low‐dose exposure to DEHP during adolescence on sperm function in adult rats. The male rats were daily gavaged with 30, 100, 300, and 1000 µg kg^?1 of DEHP or corn oil from postnatal day (PND) 42 until PND 105. The selection of DEHP doses ranged from the mean daily intake by the normal‐population exposure levels to no‐observed‐adverse‐effect level of DEHP for the endpoints evaluated until adulthood. Significant increases in the percentage of sperm with tail abnormality, tendency for sperm DNA fragmentation index (DFI) and percentage of sperm with DFI were found in those exposed to 100, 300, and 1000 µg kg^?1 (P < 0.05). We observed a significant increase of hydrogen peroxide (H₂O₂) generation in the sperm of the 1000 µg kg^?1 group compared with the control group (P < 0.05). The excessive production of sperm H₂O₂ coincided with an increase in sperm DFI. In this study, the lowest‐observed‐adverse‐effect level for sperm toxicity was considered to be 100 µg DEHP/kg/day in sperm morphology and chromatin DNA damage. Further research is necessary to clarify the mechanisms of DEHP‐related sperm ROS generation on sperm DNA damage. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 706–712, 2016.     

Disobutamide-induced cytoplasmic vacuoles in cultured dog coronary artery muscle cells

Smooth muscle cells released by protease from the coronary artery of dogs were cultured in M199 supplemented with 10% fetal calf serum. Cells were grown on glass coverslips to semiconfluence and exposed to disobutamide at 0,1, 2, 3, 6, 8, and 10 × 10^–4 M for 24, 48, and 72 h, examined in situ by light microscopy, then fixed in 100% methanol, stained with May-Grünwald Giemsa and examined by light microscopy. Cells were also exposed to drug for 24 h, pelleted, fixed and prepared routinely for electron microscopy. Control cells and cells exposed to 6 × 10^–4 M disobutamide were examined. Vacuole formation was dose and time dependent between 2 x 10^–4 M and 10^–3 M. By light microscopy, morphologic alterations induced by the drug were clear cytoplasmic vacuoles in live cells, vacuoles in dead cells and dead cells without vacuoles. Small round vacuoles were an early change. Dark granules were dispersed among the vacuoles. The vacuoles increased in size at higher doses or longer times. Eventually all the cytoplasm was occupied by vacuoles and the cells were enlarged. By electron microscopy, the vacuoles were round, primarily membrane-bound, contained mostly electron-lucent material and occasionally small flocculent bodies. There was vacuolar coalescence. The dose response of vacuole induction in confluent and semiconfluent cells was similar. Cytoplasmic vacuoles without cell death can be induced by disobutamide at 2 or 4 × 10^–4 M during a 3-day exposure. Cell culture is a suitable biological system for studying cytoplasmic vacuoles of the type induced by disobutamide.Presented in part as an Abstract (# 2924) in the 1983 Annual Meeting of the Fed. Am. Soc. Exp. Biol., April 10–14, 1983, Chicago, Illinois, and published in Fed. Proc. 42(4): 972.     

Ovotoxicity and PPAR-mediated aromatase downregulation in female Sprague-Dawley rats following combined oral exposure to benzo[a]pyrene and di-(2-ethylhexyl) phthalate

The aim of the present study was to determine the ovotoxicity of female Sprague-Dawley (SD) rats exposed to benzo[a]pyrene (B[a]P) and di-(2-ethylhexyl) phthalate (DEHP), either alone or in combination; the molecular mechanism and the combined effects were also evaluated. Female rats were given intragastric administration of control (corn oil), B[a]P (5 and 10mg/kg), DEHP (300 and 600 mg/kg) and B[a]P+DEHP (at 5mg/kg and 300 mg/kg respectively, or at 10mg/kg and 600 mg/kg respectively) on alternate days for 60 days. Relative ovary weight, estrous cycle, 17β-estradiol blood level, ovarian follicle populations, granulosa cell apoptosis, and gene and protein expression of P450Arom and PPAR were investigated. Our study demonstrated that the combination of B[a]P and DEHP exerts ovotoxicity in female rats and suppression of sex hormone secretion and homeostasis, which is associated with prolonged estrous cycles, decreases in ovarian follicle populations and granulosa cell apoptosis involving a PPAR-mediated signaling pathway of action of the two chemicals. In addition, based on qualitative assessment of the combined toxicity, no interaction effects were observed following combined B[a]P and DEHP administration.     

柚皮苷调控心肌PPARγ表达对实验性2型糖尿病心肌病大鼠模型心肌损伤的防治作用

目的探讨过氧化物酶体增殖因子活化受体γ(PPARγ)在实验性2型糖尿病心肌病大鼠模型心肌结构功能损伤中的作用;柚皮苷治疗能否减轻心肌结构功能损伤及其可能的机制。方法 6周龄♂Wister大鼠80只建立实验性2型糖尿病心肌病模型,随机分为模型对照组、柚皮苷高、中、低剂量治疗组、PPARγ激动剂吡格列酮治疗组(各组16只),正常大鼠16只作为正常对照。观察不同剂量柚皮苷口服(40、20、10 mg.kg-1.d-1)治疗对心肌结构功能损伤程度的影响;免疫组化检测心肌PPARγ表达、免疫荧光定量检测外周血B型脑钠肽(BNP)和心肌肌钙蛋白I(cTnI)蛋白表达;透射电镜观察心肌细胞超微结构。结果①PPARγ在模型对照组表达增强,主要定位在血管内皮细胞及心肌细胞胞质区;相比于空白对照,模型对照组葡萄糖耐量(OGTT)阳性,心肌病损指标(心脏/体重指数、FFA、HO-MA-IR、GSP、BNP)均增高,心肌细胞超微结构损伤明显;②相比于模型对照组,中、高剂量柚皮苷和吡格列酮治疗组PPARγ表达下调,PPARγ阳性光密度呈阳性也减弱,相应灰度值增加(P<0.05);心脏/体重指数、FFA、HOMA-IR、GSP、BNP下调;OGTT及心肌细胞超微结构损伤明显改善;③相比于吡格列酮治疗组,高剂量柚皮苷治疗组在下调BNP方面明显,但改善HOMA-IR方面较差(P<0.05)。结论柚皮苷治疗减轻糖尿病心肌病心肌结构功能损伤,其机制可能与调控心肌PPARγ表达介导改善胰岛素抵抗、阻断FFA活化、抑制B型脑钠肽表达作用有关。