白细胞介素11防治大鼠大剂量甲氨蝶呤致黏膜炎的实验研究

目的　观察白细胞介素 11(IL 11)防治大剂量甲氨蝶呤 (HDMTX)致Wistar大鼠小肠黏膜炎的疗效及IL 11对HDMTX抑制人T淋巴细胞白血病细胞系CEM增殖作用的影响。方法　Wistar大鼠腹腔注射MTX 1ml(10 0mg/kg) ,同时皮下注射IL 114 75 μg·kg-1·d-1(大剂量 )或 15 0 μg·kg-1·d-1(小剂量 ) ,分 2次 ,共 2d ;同时设生理盐水对照组及单独注射MTX对照组。各组大鼠于MTX注射后第1,3,5 ,7天处死 ,观察各组大鼠死亡率、小肠组织形态学及超微结构变化以及小肠隐窝细胞增殖细胞核抗原 (PCNA)变化情况。MTT法观察不同浓度IL 11对CEM细胞增殖的影响及对HDMTX抑制作用的影响。结果　在体内 ,IL 11可明显降低小肠组织病理学积分 ,增加小肠绒毛的高度 ,增加绒毛高度/隐窝深度的比值 ,促进小肠隐窝细胞核的增殖 ,使实验鼠死亡率下降。IL 11预防治疗组效果最好 ,与MTX对照组比较 ,差异有统计学意义 (P <0 .0 1)。在体外 ,IL 11对CEM细胞的增殖及HDMTX的抑瘤作用无明显影响。结论IL 11可以明显减轻HDMTX诱发的小肠黏膜炎的严重程度 ,缩短病程 ,提高实验动物的存活率 ,IL 11可以安全地用于儿童急性淋巴细胞白血病HDMTX的化疗。     

抑肽酶对实验性慢性肝损伤的保护作用

目的探讨抑肽酶对实验鼠慢性肝细胞损伤的保护作用。方法利用四氯化碳建立Wister大鼠慢性肝损伤实验动物模型，并给予抑肽酶观察其对实验鼠血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、白蛋白（ALB）、白蛋白臁蛋白（A／G）、唾液酸（SA）、胆碱酯酶（CHE）、碱性磷酸酶（ALP）、γ-谷氨酰转移酶（γ-G）、总胆红素（TBIL）含量、肝组织羟脯氨酸（hydroxyproline，Hyd）含量及肝组织的病理改变的影响。结果抑肽酶明显降低血清ALT、AST、ALP、γ-G、T-BIL，明显增高血清ALB、A／G、SA、CHE值。肝组织Hyd含量明显降低。鼠肝组织病理性改变明显减轻。结论抑肽酶对大鼠慢性肝损伤具有明显的保护作用。     

乌司他丁对心肺复苏后Wistar鼠大脑皮层炎症反应的影响

目的 评价乌司他丁(UTI)对心肺复苏(CPR)后大鼠大脑皮层炎症因子TNF-α和IL-6表达及神经元细胞凋亡的影响.方法 36只成年雄性Wistar大鼠采用交流电致颤的方式诱发室颤(VF),持续7 min后进行CPR,建立VF/CPR模型.自主循环恢复(ROSC)后立即给予乌司他丁100 000 U/kg或等体积的PBS静脉注射.VF前和ROSC后2、4、8h采血检测血浆TNF-α、IL-6水平,并取大脑皮层进行定量PCR和Western blot检测TNF-α、IL-6 mRNA表达和蛋白表达,检测核因子NF-κB p65的核浆转位情况.ROSC后72 h行皮层NISSL和TUNEL染色计数顶叶皮层存活神经元细胞数和凋亡神经元细胞数.结果 ROSC后UTI组2、4、8h血浆TNF-α质量浓度分别为(17.7±1.4)、(21.9±2.1)和(17.1±0.6),低于PBS组(t2h=1.42,t4h =2.93,t8 h =4.22,各组P＜0.05).UTI组2、4、8h血浆IL-6质量浓度(ng/mL)分别为(208.9±14.1)、(281.5 ±25.9)和(251.8±15.3),显著低于PBS组(t2h=3.87,t4h=2.45,t8h=3.74,各组P＜0.05).ROSC后UTI组2、4、8h大脑皮层TNF-α、IL-6 mRNA表达和蛋白表达量均显著低于PBS组.PBS组ROSC后2、4、8h大脑皮层NF-κB p65的核/浆转换率为(1.08±0.08)、(1.02±0.05)和(0.97 ±0.02),高于UTI组.ROSC后72 h UTI组大脑皮层存活神经元细胞数为(22±3)个/400×400像素,多于PBS组的(19±2)个/400×400像素(Z=2.887,P=0.02);凋亡细胞数UTI组为(10±2)个/400×400像素,低于PBS组的(13±3)个/400×400像素(Z =3.751 P=0.01).结论 UTI降低ROSC后Wistar大鼠全身炎症反应,减少大脑皮层NF-κB通路的激活,减少致炎因子TNF-α和IL-6的表达,从而减少神经元细胞凋亡,促进细胞存活.     

Antitumour and toxic effects on Wistar rats of two new platinum complexes

BACKGROUND: Cancer chemotherapy in humans based on metal complexes started at the clinical level in the late 1970s with the use of cisplatin, which forms intra-strand cross-links with DNA. METHODS: Two new platinum complexes of cis-geometry with the amino acids inosine (ino) and l-alanine (ala), Pt(ino)2Cl2 and cis-[Pt(NH3)2(ala)](NO3), respectively, were synthesized and pure samples were obtained by means of flash chromatography. These complexes were tested on benzo(a)pyrene-induced tumours in Wistar rats to detect their antitumour and toxic effects. RESULTS: There was a statistically significant prolongation of the mean survival time of the animals in the two groups tested (272 +/- 18 days and 246 +/- 26 days, respectively) compared to the control group (195 +/- 22 days) (P < 0.001). Toxic effects included a decrease in leucocyte cell count, mild haemolysis, mild haematuria, mild hepatotoxicity, elevated body temperature and hair loss. All of these effects were reversible after drug discontinuation. CONCLUSIONS: The two new platinum complexes described here appear to have an effective antitumour activity without severe toxicity when tested on Wistar rats.     

高脂低碳水化合物膳食模式对肥胖大鼠影响的研究

目的探讨高脂低碳水化合物膳食模式对肥胖大鼠影响。方法利用膳食模式建立营养性肥胖大鼠模型100只,用随机数字表法按体重分层随机分为普通饲料对照组20只(9.0%脂肪,78%碳水化合物)、高脂饲料组80只(70%脂肪,16%碳水化合物)。每天称进食量;每周称大鼠体重;第3和第11周测血脂;第10周进行口服葡萄糖耐量试验和胰岛素释放试验、第11周测瘦素和酮体。结果两组大鼠原摄食标准为85 g/3 d,对照组大鼠3 d内85 g食物全部食用,观察组大鼠摄食量明显下降,摄入能量减少,且与对照组比较差异有统计学意义(P0.05);观察组大鼠高脂低碳水化合物膳食模式进行第28天、第35天、第42天、第56天、第70 d体重增长明显,且与对照组同时间段比较差异均有统计学意义(P0.05);观察组大鼠高脂低碳水化合物膳食模式进行到第9周后甘油三酯(TG)、总胆固醇(TC)明显高于对照组同期水平、而高密度脂蛋白胆固醇(HDL-C)明显低于对照组,且差异均有统计学意义(P0.05);与对照组比较,观察组大鼠高脂低碳水化合物膳食模式进行70 d后,体重、脂肪垫重、Lee氏指数、脂肪体比等指标明显升高,脾体比明显降低,差异均有统计学意义(P0.05);观察组大鼠观察组在15 min餐后血糖水平明显高于对照组,且与比较差异有统计学意义(P0.05);两组大鼠喂养70 d后瘦素、酮体等指标比较差异无统计学意义(P0.05)。结论高脂低碳水化合物膳食模式使大鼠对脂代谢的调节能力下降,出现血脂紊乱。     

不同高脂饲料对小鼠肥胖和胰岛素抵抗模型制备情况的效果比较

目的:探讨两种不同的高脂饲料在C57/BL6J小鼠肥胖和胰岛素抵抗(IR)模型制备过程中的效果差别,以期为更好的制备C57/BL6J小鼠肥胖和IR模型提供理论指导.方法:以雄性C57/BL6小鼠为实验材料,随机分为三组,分别为基础组,喂食国内A公司啮齿动物基础饲料;模型1组,喂食国内A公司生产的啮齿动物高脂饲料(HFD...     

Cachexia in chronic kidney disease: a link to defective central nervous system control of appetite

Anorexia is one of several abnormalities characterizing chronic kidney disease (CKD) that cause cachexia, the loss of muscle and adipose stores. It has been attributed to mechanisms ranging from accumulation of toxic "middle molecules" to psychological problems. In this issue of the JCI, Cheung and coworkers used elegant techniques to demonstrate that CKD-associated anorexia is caused by defective hypothalamic regulation of appetite. They attributed the defect to an alteration in the hypothalamus's response to leptin and inflammation. Since similar hypothalamic defects suppress appetite in inflammatory states and in cancer, it is possible that anorexia in several cachexia-inducing conditions results from a common set of hypothalamic abnormalities. The development of small molecules capable of preventing these regulatory abnormalities holds the promise of eliminating the contribution of anorexia to the development of cachexia.     

Anti-diarrhoeal and ulcer-protective effects of violacein isolated from Chromobacterium violaceum in Wistar rats

Violacein was isolated from Chromobacterium violaceum , a soil Gram-negative bacterium collected from the forest water body soil sample from Kolli Hills of Tamil Nadu, India. In the present study the anti-diarrhoeal and ulcer-protective properties of violacein were investigated in Wistar rats using castor oil, magnesium sulphate and ethanol. The intestinal transit in rats was significantly ( P  < 0.001) reduced and gastric emptying was delayed; 40 mg/kg of violacein elicited a greater anti-motility activity than 0.1 mg/kg of atropine. Violacein exhibited ulcer-protective properties against ethanol-induced ulceration in rats with maximal anti-ulcer activity at 40 mg/kg. Violacein also exerted significant anti-enteropooling effects, causing a dose-related inhibitory effect on castor oil-induced enteropooling in rats. A profound anti-diarrhoeal activity was observed when violacein was tested in diarrhoeic rats. The frequencies of defaecation as well as the wetness of the faecal droppings were significantly reduced. Furthermore, violacein (40 mg/kg) produced 87.84% inhibition of castor oil-induced diarrhoea in rats. The results suggested that violacein can be used for the treatment of diarrhoeal and ulcer-related diseases.     

高脂饲料对大鼠体质量及毛发变化的影响

目 的 ： 观 察 和 分 析 高 脂 饲 料 对 ＳＤ 大 鼠 体 质 量 下 降 和 毛 发 变 化 的 影 响 ，为 高 脂 血 症 的 康 复 干 预 提 供 实 验 学 依 据 。方 法 ：实 验 于 ２００２－０３／０７在 新 乡 医 学 院 形 态 中 心 实 验 室 进 行 ，取 雄 性ＳＤ 大 鼠 ６０只 ，采 用 随 机 数 字 法 分 为 实 验 组 和 对 照 组 （ｎ ＝３０）。 实 验 组高 脂 饲 料 ，对 照 组 普 通 颗 粒 饲 料 喂 养 ，两 组 均 自 由 饮 水 。 分 别 于 高 脂 饲料 后 ７，３０和 ９０ｄ，用 婴 儿 秤 称 量 大 鼠 体 质 量 ，并 观 察 毛 发 改 变 情 况 。结 果 ：高 脂 饲 料 后 ７ｄ 实 验 组 大 鼠 体 质 量（ １３５．５±２３．４）ｇ，与 对 照 组 大鼠 体 质 量 （１３９．９ ±１５．５） ｇ 无 差 异 。 ３０ ｄ 时 实 验 组 平 均 体 质 量（１４７．４±２４．７）ｇ，低 于 对 照 组 平 均 体 质 量 （１７１．９±３３．１）ｇ，两 组 间 差异 有 显 著 性 意 义 （ｔ＝２．２６，Ｐ ＜０．０５）；毛 发 脱 落 。９０ｄ 时 实 验 组 体 质 量为 （１１６．７± １７．５）ｇ，明 显 低 于 对 照 组 （４０８．０±２７．５）ｇ，脱 毛 严 重 。结 论 ：高 脂 饲 料 可 引 起 ＳＤ 大 鼠 体 质 量     

胰岛素对大鼠脑缺血再灌注时神经元凋亡及其相应基因的调控

目的观察胰岛素(insulin,RI)对缺血再灌注损伤后细胞凋亡及其相应基因的调控作用,评估RI对脑缺血再灌注损伤的保护作用。方法将健康wistar大鼠56只,随机分为对照组、缺血再灌注盐水组(NS)、缺血再灌注胰岛素组(RI)。采用pulsinelli4血管阻塞模型,观察RI、NS在4,24,48h海马CA1区存活神经元数目,TUNEL阳性细胞数目,Bcl-2蛋白的表达,以观察比较缺血再灌注阶段细胞凋亡的变化。结果再灌注NS组CA1区神经元数目(36±6)个/mm2较再灌注RI组(88±9)个/mm2少(t=3.34,P<0.01)。再灌注后CA1区细胞凋亡数:4h时再灌注NS组(12±3)个/mm2高于再灌注RI(8±1)个/mm2和假手术组(2±1)个/mm2:组间比较,F=127.66,P<0.001。Bcl-2对海马CA1细胞凋亡评估4h时,再灌注NS组43.0±9.8,高于再灌注RI组24.0±5.4和假手术组2.7±0.8。结论全脑缺血再灌注时急用RI可减轻脑缺血再灌注神经元凋亡,对脑缺血再灌注损伤引起的神经元延迟性坏死有保护作用。     

The effects of hyperinsulinaemia on myocardial mass, blood pressure regulation and central haemodynamics in rats

Left ventricular hypertrophy is a condition with high mortality. An association with insulin resistance and hyperinsulinaemia has recently been suggested. The aim of this study was to examine the effects of isolated hyperinsulinaemia on cardiac weight and haemodynamic regulation. Rats were exposed to hyperinsulinaemia for 7 weeks after adrenalectomy with corticosterone substitution and continuous infusion of propranolol to control counter-regulatory mechanism ( n =15) (AIP group). Hypoglycaemia was prevented by glucose in the drinking water. Hyperinsulinaemic (AIP) rats were heavier and had increased relative masses of the myocardium (left ventricle 17% and right ventricle 20%), kidneys and adipose tissues in comparison with normoinsulinaemic adrenalectomized, corticosterone- and propranolol-treated controls (AP) ( n =10). Blood pressure in the insulin-exposed animals, measured weekly by the tail-cuff method in conscious rats, was not different from (AP) controls over 5 weeks, but increased in the sixth week. At the end of the seventh experimental week, blood pressure measured intra-arterially was also found to be elevated. Heart rate was not changed but total peripheral resistance was about twice that of controls ( P <0.001). Cardiac output and stroke volume was 30–40% lower in the AIP rats ( P <0.05). It is concluded that exposure to elevated insulin levels with control of counter-regulating mechanisms from β-adrenergic mechanisms and adrenals is not immediately followed by blood pressure elevation. It is, therefore, suggested that early onset of blood pressure elevation after insulin exposure might be caused by insulin counter-regulatory events, causing both insulin resistance and blood pressure elevation. The long-term adaptations may involve a direct influence by insulin as a 'trophic factor' on myocardial and on peripheral resistance vessels, followed by increased blood pressure, decreased cardiac output and stroke volume.     

Chronic pain: a PET study of the central effects of percutaneous high cervical cordotomy.

We have studied 5 patients with unilateral, severe chronic pain due to cancer before and after percutaneous, ventrolateral cervical cordotomy to investigate the central effects of the procedure. The aim was to identify the functional anatomical correlates of abolishing unilateral nociceptive input to the brain. Patients were investigated by positron emission tomography using C15O2 to evaluate cerebral blood flow. Comparisons were made between the patients with unilateral pain before cordotomy and normal volunteers. These demonstrated significantly less blood flow in 3 out of 4 of the individual quadrants of the hemithalamus contralateral to the side of pain (P less than 0.01-0.05). These differences were abolished by cordotomy. Comparison of the patients before and after cordotomy showed a significant decrease in blood flow in the dorsal anterior quadrant of the thalamus contralateral to the side of pain (P less than 0.05) which was normalised after cordotomy. There were no significant changes in the prefrontal or primary somatosensory cortex. We conclude that chronic pain results in a decrease of synaptic activity at thalamic level either from decreased activity in neurones projecting to that region and/or attenuated local neuronal firing. We have demonstrated no secondary remote effects in cortex, indicating the importance of subcortical mechanisms in central responses to chronic pain.     

The pursuit of a high central venous oxygen saturation in sepsis: growing concerns

In this issue of Critical Care, Dutch investigators report that, in a cohort of patients with sepsis/septic shock admitted to three different intensive care units (ICUs), low central venous oxygen saturation (ScvO₂) was uncommon at the time of ICU admission, and hospital mortality was <30%. Their findings, taken together with those of recent reports from Australia and New Zealand (ANZ), raise serious concerns about the utility of early goal directed therapy (EGDT) outside the context of the original trial. Despite inclusion of EGDT into the Surviving Sepsis Guidelines, in response to growing uncertainty, ANZ and US investigators will soon begin randomization of patients into two large multicentre trials comparing EGDT to standard therapy. Until such studies are completed, basing international treatment guidelines on a single centre study performed in what may turn out to be a highly atypical environment would seem premature.     

The 90-day oral toxicity of d-psicose in male Wistar rats

d-Psicose is a rare sugar present in small quantities in natural products. In a previous study, we showed that d-psicose suppresses increase in plasma glucose and reduces body fat accumulation in rats. Based on acute toxicity testing in rats, d-psicose is classified as an ordinary substance (LD₅₀ = 16 g/kg). Elucidating the effects of sub-chronic feeding of d-psicose in rats is essential before it can be utilized as a physiologically functional food. In this study, male Wistar rats (3 weeks old) were fed diets containing 3% d-psicose or sucrose for 90 days. The body weight gain and intra-abdominal adipose tissue weight did not differ between the sucrose and the d-psicose groups. The weights of the liver and kidneys were significantly higher in the d-psicose group than in the sucrose group. However, no gross pathological findings were evident at dietary doses of 3% d-psicose or were correlated with hypertrophy of the liver and kidney. In a clinical chemistry analysis, the erythrocyte and leukocyte courts were significantly higher in the d-psicose group, but that was not considered to be toxicologically significant. Therefore, the present study found no adverse effects of d-psicose in rats fed a diet containing 3% d-psicosefor 90 days.     

吸烟对大鼠尿液中若干促石、抑石成分的影响研究

目的：了解吸烟对Wistar大鼠尿液生化指标的影响。方法：健康雄性Wistar大鼠168只，分成吸烟5支/d组、吸烟10支/d组和空白对照组，均饮用超纯净水，观察第0、10、20、30、40、50、60天时，各组大鼠尿草酸、枸橼酸、钙、钠水平。结果：随吸烟时间的延长，大鼠尿枸橼酸水平逐渐降低。结论：吸烟能够降低成石抑制物的排泄水平。     

高脂饮食诱导胰岛素抵抗小鼠骨骼肌胰岛素信号通路相关基因表达的变化

目的:利用基因芯片技术研究高脂饮食诱导的胰岛素抵抗(insulin resistance,IR)小鼠骨骼肌细胞胰岛素信号通路相关基因的改变,分析其变化规律,为寻找治疗IR的潜在药物作用靶点提供理论依据。方法:选用雄性C57BL/6小鼠40只,随机分为正常饮食组(NC组)和高脂饮食组(HC组)。分别饲养16周后,采用口服糖耐量试验(oral glucose tolerance test,OGTT)检测小鼠葡萄糖耐量;ELISA检测空腹血清胰岛素值(fasting insulin,FIN)以确定胰岛素抵抗模型成功;后分离小鼠股四头肌,提取总RNA,经过荧光标记后进行基因芯片杂交,利用芯片扫描仪记录荧光信号,并通过相关软件对所得数据进行统计学分析。结果:16周高脂饮食喂养结束后,HC组小鼠体重较NC组增加25.33%(P<0.05),FIN值较NC组增加77.19%(P<0.05)。OGTT峰值出现的时间较NC组延迟,血糖值在30min后下降缓慢,且在180min血糖值仍高于基础水平。胰岛素信号通路的差异表达基因有11个。表达上调的基因有3个,表达下调的基因有8个,这些基因涉及糖代谢、脂代谢、信号转导及转录等生物学过程。结论:16周的高脂饮食可以诱发C57BL/6小鼠产生IR。HC组小鼠骨骼肌胰岛素信号相关基因发生差异表达,这些基因与IR密切相关。本研究为寻找治疗IR潜在的药物靶点提供理论依据。     

高血糖对Wistar大鼠肾脏组织MMP-9mRNA、MMP-9蛋白表达的影响

目的:观察高血糖对Wistar大鼠肾脏基质金属蛋白酶9(MMP-9)mRNA、MMP-9蛋白表达的影响。方法:将40只雌性大鼠随机分为空白对照组(5只)和糖尿病组(DM组,35只)。糖尿病组用链脲佐菌素(STZ)一次性腹腔注射造模,造模成功后再次随机分组为5组,每组5只(余因造模未成功或死亡而被剔除)。5组分别为造模成功后第1天、第3天、第7天、第10天和第14天处死组,期间各组大鼠未予任何药物干预。处死大鼠后取其肾脏组织,用荧光定量PCR(FQ-PCR)法检测各组肾脏组织MMP-9mRNA的变化,免疫组化法观察肾小球基底膜区MMP-9蛋白变化。结果:①空白对照组和DM组大鼠肾脏组织中均有MMP-9mRNA表达,空白对照组与DM各组相比,MMP-9mRNA表达水平差异均无统计学意义(P>0.05)。血糖水平、高糖持续时间与MMP-9mRNA表达量均不相关。②免疫组化提示,DM组MMP-9蛋白在肾小球内主要表达于基底膜,以第7天处死组大鼠肾脏肾小球基底膜区MMP-9着色最强。定量分析示,第7天处死组大鼠肾脏肾小球基底膜区MMP-9蛋白水平达峰值,且血糖水平及高血糖持续时间与MMP-9蛋白水平呈正相关。结论:①DM大鼠肾脏组织内MMP-9mRNA不受血糖水平、高血糖持续时间等因素影响。②DM大鼠肾脏组织肾小球基底膜区MMP-9蛋白水平于成功造模后第7天第1次达峰值,且其MMP-9蛋白水平与血糖水平、高血糖持续时间呈正相关。     

高脂饮食对大鼠非酒精性脂肪肝中解偶联蛋白2的诱导作用

背景:至今非酒精性脂肪肝的发病机制不十分清楚,而线粒体膜上的解偶联蛋白可使线粒体氧化磷酸化解偶联,导致线粒体合成ATP效率降低,通过能量代谢的改变,参与脂肪肝的发生。目的:观察解偶联蛋白2在大鼠非酒精性脂肪肝动物模型各时相点的表达规律。设计:随机对照动物实验。单位:解放军第三军医大学大平医院野战外科研究所消化科。材料:实验于2004-11/2005-12在解放军第三军医大学大坪医院野战外科研究所国家重点实验室进行。取清洁级Wistar成年雄性大鼠64只,普通饲料正常喂养1周后,随机分为模型组和正常对照组2组,每组32只,每组又分饲养2,4,8,12周4个时间点,每个时间点8只。方法:模型组大鼠喂高脂饮食(基础饲料88%、猪油10%、胆固醇2%)饲养12周,正常对照组普通饲料喂养,分笼(每笼6只)饲养。主要观察指标:两组于相应时间点麻醉后采血,处死动物,迅速取出肝脏。①免疫组织化学和Westernblot技术检测肝组织中解偶联蛋白2表达变化。②生化检测大鼠血清三酰甘油、游离脂肪酸和丙氨酸氨基转移酶活性。③检测肝组织丙二醛含量。结果:64只大鼠全部进入结果分析。①血清生化指标:模型组饲养4,8,12周时血清三酰甘油、游离脂肪酸和丙氨酸氨基转移酶水平明显高于正常对照组,以8,12周最显著(P<0.01)。②模型组解偶联蛋白2蛋白表达随脂肪肝程度的加重,其表达逐渐增强,而正常对照组几乎阴性表达。③肝组织丙二醛含量:模型组饲养4,8,12周明显高于正常对照组,以8,12周最显著[(4.07±0.15),(4.93±0.14),(5.20±0.20)μmol/g;(3.14±0.20),(3.12±0.18),(3.13±0.16)μmol/g,P<0.01]。结论:随着非酒精性脂肪的形成和程度加重,血清三酰甘油、游离脂肪酸和丙氨酸氨基转移酶及肝组织丙二醛含量增加,解偶联蛋白2表达也逐渐增强,提示高脂饮食可诱导肝细胞表达解偶联蛋白2,使细胞内ATP生成减少,促进脂肪肝的形成和发展。