EFFECT OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR ACTIVATORS ON TUMOR NECROSIS FACTOR-αL EXPRESSION IN NEONATAL RAT CARDIAC MYOCYTES A

Objecfive To investigate the effect ofperoxisome proliferator-αctivated receptor-α (PPARα) and PPARγ activators on tumor necrosis factor-α (TNFα) expression in neonatal rat cardiac myocytes. Primary cultures of cardiac myocytes from 1- to 3-dayold Wistar rats were prepared, and myocytes were ex-posed to lipopolysaccharide (LPS) and varying concentrations of PPARα or PPARγ activator (fenofibrate or pioglitazone).RT-PCR and ELISA were used to measure TNFα, PPARα, and PPARγ expression in cultured cardiac myocytes. Transient transfection of TNFα promoter with or without nuclear factor-kappaB (NF-κB) binding site to cardiac myocytes was performed. Performed Pretreatment of cardiac myocytes with fenofibrate or pioglitazone inhibited LPS-induced TNFα mRNA and protein expression in a dose-dependent manner. However, no significant changes were observed on PPARα or PPARα mRNA expression when cardiac myocytes were pretreated with fenofibrate or pioglitazone. Proportional suppression of TNFα promoter activity was observed when myocytes was transiently transfected with whole length of TNFα promoter (-721/ 17) after being stimulated with LPS and fenofibrate or pioglitazone, whereas no change of promoter activity was observed with transfection of TNFα reporter construct in deletion of NF-κBbinding site (- 182/ 17). Conchusions PPARα and PPARγ activators may inhibit cardiac TNFα expression but not accompanied by change of PPARα or PPARγ mRNA expression. Therefore PPARα and PPARγ activators appear to play a role in anti-inflammation.The mechanism may partly be involved in suppression of the NF-κBpathway.     

EFFECT OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR ACTIVATORS ON TUMOR NECROSIS FACTOR-α EXPRESSION IN NEONATAL RAT CARDIAC MYOCYTES

Objective To investigate the effect ofperoxisome proliferator-activated receptor-α (PPARα) and PPARγ activators on tumor necrosis factor-α (TNFα) expression in neonatal rat cardiac myocytes.Methods Primary cultures of cardiac myocytes from 1- to 3-day-old Wistar rats were prepared, and myocytes were exposed to lipopolysaccharide (LPS) and varying concentrations of PPARα or PPARγ activator (fenofibrate or pioglitazone).RT-PCR and ELISA were used to measure TNFα, PPARα, and PPARγexpression in cultured cardiac myocytes. Transient transfection of TNFα promoter with or without nuclear factor-kappaB (NF-κB) binding site to cardiac myocytes was performed.Results Pretreatment of cardiac myocytes with fenofibrate or pioglitazone inhibited LPS-induced TNFα mRNA and protein expression in a dose-dependent manner. However, no significant changes were observed on PPARα or PPARγ mRNA expression when cardiac myocytes were pretreated with fenofibrate or pioglitazone. Proportional suppression of TNFαpromoter activity was observed when myocytes was transiently transfected with whole length of TNFα promoter (-721/ 17) after being stimulated with LPS and fenofibrate or pioglitazone, whereas no change of promoter activity was observed with transfection of TNFα reporter construct in deletion of NF-κB binding site (-182/ 17).Conclusions PPARα and PPARγ activators may inhibit cardiac TNFα expression but not accompanied by change of PPARα or PPARγmRNA expression. Therefore PPARα and PPARγ activators appear to play a role in anti-inflammation.The mechanism may partly be involved in suppression of the NF-κB pathway.     

The Different Expression of PPARγ in the Artery Tissues of Hypertensive Patients with Different Ages

Objective: To study the expression of the peroxisome proliferator-activated receptor γ(PPARγ) in the artery tissues of essential hypertensive patients, and the different changes with different ages, especially to the hypertensive patients more than 65 years old.Methods: Collected the mesenteric artery tissues of essential hypertensive patients( ＞65 years old group and ＜65 years old group)and patients with normal blood pressure,using immunohistochemical analysis and image acquiring and analysis system to detect the expression of PPARγ in the artery tissues. Results: the expression of PPARγ in the artery tissues of essential hypertensive patients is higher than that in the patients with normal blood pressure( P ＜ 0.05), and to the group of hypertensive patients, the expression of PPARγ in ＞ 65 years old group is higher than that in ＜ 65 years old group ( P ＜ 0.05). Conclusion: the expression of PPARγ in artery tissues is increased in hypertensive patients than in the patients with normal blood pressure, and increased with aging in hypertensive patients, suggesting that PPARγhas great relationship with hypertension.     

The Different Expression of PPARγ in the Artery Tissues of Hypertensive Patients with Different Ages

Objective： To study the expression of the peroxisome proliferator-activated receptor γ（PPARγ） in the artery tissues of essential hypertensive patients, and the different changes with different ages, especially to the hypertensive patients more than 65 years old. Methods： Collected the mesenteric artery tissues of essential hypertensive patients（ 〉 65 years old group and 〈 65 years old group）and patients with normal blood pressure, using immunohistochemical analysis and image acquiring and analysis system to detect the expression of PPARγ in the artery tissues. Results： the expression of PPARγ in the artery tissues of essential hypertensive patients is higher than that in the patients with normal blood pressure（ P 〈 0.05）, and to the group of hypertensive patients, the expression of PPARγ in 〉 65 years old group is higher than that in 〈65 years old group （P〈0.05）. Conclusion： the expression of PPARγ in artery tissues is increased in hypertensive patients than in the patients with normal blood pressure, and increased with aging in hypertensive patients, suggesting that PPARγ has great relationship with hypertension.     

Effects of angiotensin Ⅱ receptor antagonist on expression of collagen Ⅲ, collagen Ⅴ, and transforming growth factor β1 in the airway walls of sensitized rats

Background Repeated attacks of bronchial asthma lead to different degrees of airway remodeling, the mechanism of which is not yet clear. Some evidences indicate that it is related to the excessive expression of some growth promotion factors. Angiotensin Ⅱ is a polypeptide that may be involved in airway remodeling. To evaluate its role in airway remodeling in asthma, we observed the effects of an angiotensin Ⅱ type 1 receptor antagonist (valsartan) on the expression of collagen Ⅲ, collagen Ⅴ, and transforming growth factor β1 (TGF-β1) mRNA and protein in the airway walls of sensitized rats.Methods Forty Wistar rats were randomly divided into 5 groups: control group, sensitized group, and valsartan groups 1, 2, and 3. The rats in the sensitized group and in valsartan groups 1, 2, and 3 were sensitized and challenged with ovalbumin. Rats in control group were sensitized and challenged with 0.9% NaCl. Rats from valsartan groups 1, 2, and 3 were drenched with valsartan (10 μg, 20 μg, or 30 μg, respectively) at the time of the ovalbumin challenges. The expression of collagen Ⅲ, collagen Ⅴ, and TGF-β1 protein were detected using immunohistochemical method in combination with image analysis methods. The expression of TGF-β1 mRNA was detected by in situ hybridization. Results The expression in the airways of collagen Ⅲ and collagen Ⅴ was significantly higher in rats from the sensitized group (7.73±0.81, 1.34±0.28) and from valsartan groups 1, 2, and 3 (5.73±0.64, 1.13±0.15; 4.96±0.51, 0.98±0.08; 4.43±0.35, 0.93±0.06, respectively) than those in the control group (2.65±0.38, 0.67±0.08, P<0.05). In addition, collagen levels were significantly lower in valsartan groups 1, 2, and 3 than those from the sensitized group (P<0.05). The expression of TGF-β1 mRNA and protein in the airways was significantly higher in rats from the sensitized group (20.49%±3.46%, 29.73%±3.25%) and from valsartan groups 1, 2, and 3 (16.47%±1.94%, 19.41%±1.87%; 14.38%±1.58%, 18.29%±1.43%; 12.96%±1.73%, 18.63%±1.11%, respectively) than that from the control group (7.84%±1.61%, 5.63%±1.07%, P<0.05). TGF-β1 mRNA and protein levels were significantly lower in valsartan groups 1, 2, and 3 than that in the sensitized group (P<0.05). Conclusions Angiotensin Ⅱ receptor antagonist valsartan can suppress synthesis of collagen Ⅲ and collagen Ⅴ by downregulating TGF-β1 mRNA and protein expression. Valsartan can decrease airway remodeling and could play a role in asthma therapy.     

Modulation of transforming growth factor β to platelet-derived growth factor receptor-α of human osteoblasts

Objective To investigate the mechanism and the significance of TGFβ in modulating the expression of Platelet-Derived Growth Factor Receptor-α (PDGFR-α) in human osteoblasts. Methods The osteoblasts were isolated from human fetal calvaria. The percentage of cell increase (PCI) in every 4 hours was calculated to demonstrate the proliferation of osteoblasts affected by PDGF-AA and TGFβ. The osteoblasts were cultured with TGFβ for 24 hours and with PDGF-AA for another 24 hours, and the cells proliferation was shown by PCI too. The osteoblasts were cultured with TGFβ for 24 h, and the PDGFR-α of the cells were measured by immunofluorescent analysis.Results PCI was increased by 48.2% and 22.4% after PDGF-AA and TGFβ were added into the medium for 24 hours respectively (P<0.05), and PCI decreased after the removal of the two cytokines. Preincubated with TGFβ for 24 hours and then stimulated with PDGF-AA, PCI grew slowly. TGFβ downregulated the expression of the PDGFR-α.Conclusion TGFβ can downregulate the mitogenesis of PDGF-AA by lowering the number of PDG     

EFFECT OF OXIDIZED-LDL ON NF-κB NUCLEAR TRANSLOCATION IN AORTIC SMOOTH MUSCLE CELLS ORIGINATED FROM RATS OF DIFFERENT AGES

Objective To investigate the molecular mechanism of atherosclerosis that related to age. Methods Immunohistochemistry staining and Western blot were adopted to determine the nuclear translocation of nuclear factor-kappa B (NF-κB) and expression of platelet-derived growth factor B (PDGF-B) in smooth muscle cells(SMCs) co-cultured with low density lipoprotein (LDL), oxidized LDL (ox-LDL), and ox-LDL high density lipoprotein(HDL) originated fi‘om rats of 2 and l0 months old respectively. Fat stain was used to identify the lipid intake in SMCs. Results The optimal stimulation time ofox-LDL to SMCs was 12 hours. NF-KB intensity increased in most nuclei of SMCs that originated fi‘om rats of either 2 or l0 months old co-cultured with ox-LDL. The intensity of NF-KB and the amount of intracellular lipid taken in SMCs were more obvious in cells fi‘om 10-month-old rats than fi‘om the younger ones.Change of PDGF-B expression in SMCs was not remarkable in each group of rats. Conclusions The 10-month-old rats are more susceptive to ox-LDL than 2-month-old rats in activating nuclear translocation of NF-KB. Maybe this is one of the important reasons contributing to the difference between the older and younger rats on the initiation and development of atherosclerosis lesion. Expression of PDGF-B is not associated with the activity of nuclear translocation of NF-κB.     

非诺贝特对肝脏和肌肉肉毒碱脂酰转移酶1基因表达及胰岛素敏感性的影响

目的 探讨非诺贝特对肝脏、肌肉肉毒碱脂酰转移酶1表达及胰岛素敏感性的影响.方法 将8周龄雄性SD大鼠分为3组:正常饲养组(NC,10只)、高脂饲养组(HF,10只)、高脂饲养+非诺贝特组(FF,12只).FF组在高脂饲养的基础上给予非诺贝特50 mg·kg-1·d-1剂量进行灌胃.饲养20周时测定血清、肝脏及肌肉组织中甘油三酯(TG)含量,3组均行正常血糖高胰岛素钳夹试验,并用实时聚合酶链反应方法分析肝脏和肌肉组织中肉毒碱脂酰转移酶1(CPT-1)mRNA表达的变化.结果 高脂饲养20周时,与NC组比较,HF组血清TG增加45.0%(P＜0.01),肝脏和肌肉TG含量增加2.14倍和10.64倍(P＜0.01);正常血糖高胰岛素钳夹试验表明,HF组葡萄糖的输注率(GIR)下降61%(P＜0.01),存在明显的胰岛素抵抗;肝脏CPT-1mRNA表达无明显变化(P＞0.05)、肌肉组织CPT-1mRNA表达减少71%(P＜0.01).非诺贝特干预后血TG、肝脏TG、肌肉TG较HF组分别下降70%、81%及82%,GIR增加2.52倍,肝脏、肌肉CPT-1 mRNA表达较高脂组分别增加1倍、1.05倍.结论 非诺贝特通过上调肝脏、肌肉CPT-1 mRNA表达促进脂肪酸氧化,在改善高脂饲养SD大鼠胰岛素敏感性中起重要作用.     

成纤维细胞生长因子21参与调控非诺贝特对肝脏脂质代谢的改善作用

目的：探讨成纤维细胞生长因子21（FGF21）介导非诺贝特对小鼠肝脏脂质代谢的调控。方法：将实验小鼠分为4组,均予高脂饮食喂养：野生型对照组（WT+HFD+CTL）、野生型非诺贝特治疗组（WT+HFD+FF）、FGF21基因敲除对照组（FGF21 KO+HFD+CTL）、FGF21基因敲除非诺贝特治疗组（FGF21KO+HFD+FF）。ELISA法检测小鼠血清的FGF21及Adiponectin含量;HE与油红O染色分别用于检测肝脏组织形态学变化和脂质堆积情况;TG和TC检测试剂盒用于检测血清TG及TC的变化;qRT-PCR检测PPARα、FGF21、肝脏胆固醇调节元件结合蛋白Srebp-2、脂质氧化、分解、转运等代谢调节基因（Acaca、Acacb ABCG5、ABCG8、Cyp7a1）、PPARγ、脂联素的mRNA表达。结果：非诺贝特处理4周能显著上调小鼠肝脏PPARα和FGF21表达水平,抑制小鼠体质量增加,下调血清异常血脂水平,减轻肝脏脂质沉积状况（P ＜0.05）。非诺贝特引发的保护作用在FGF21基因缺失后出现一定程度的减弱。HE和油红O染色结果显示,敲除FGF21基因减弱非诺贝特对高脂饮食喂养小鼠肝脏脂质堆积的改善作用。在分子机制方面,非诺贝特处理能显著上调脂质氧化、分解、转运等代谢调节基因（Acacb、ABCG5、Cyp7a1等）的表达,下调Srebp-2的表达（P ＜0.05）,然而,FGF21基因缺失时,这些效应被显著抑制（P ＜0.05）。同时,FGF21基因敲除可显著抑制非诺贝特诱导的PPARγ和Adiponectin的mRNA表达上调及血清水平的Adiponectin含量升高现象（P ＜0.05）。结论：FGF21介导非诺贝特发挥抗脂肪肝病变的生物学效应。     

PPAR-α激动剂增加脂肪酸氧化改善高脂诱导的胰岛素抵抗

目的研究过氧化物酶增殖体激活受体α(peroxisome proliferation activated receptor-α,PPAR-α)激动剂对脂肪酸氧化的影响及其改善高脂诱导的胰岛素抵抗(IR)的机制.方法雄性SD大鼠随机分为三组(每组各10只),A组为饱和脂肪酸(1ard)组,B组为不饱和脂肪酸(soy)组,C组为正常对照组.大鼠饲养四周后将高脂饮食组各分为两组,高脂未干预组和苯扎贝特干预组.包头两周后检测空腹血糖、胰岛素和甘油三酯水平,并取出肝脏、肌肉和脂肪组织,检测组织肉碱脂酰转移酶-1(CPT-1)和PPAR-αmR-NA的表达,mRNA表达采用RT-PCR的方法,以β-actin作为内参照.结果肌肉和脂肪CPT-1mRNA表达在高脂未干预组明显低于苯扎贝物干预组和正常对照组,而未干预组间无显著差异.PPAR-αmRNA表达在各组间均无显著性差异.结论高脂饮食可使肌肉和脂肪组织CPT-1mRNA表达减少,而PPAR-αmR-NA激动剂苯扎贝特则可使CPT-1mRNA表达明显增加,肝脏PPAR-αmRNA表达在各组均无明显改变.这说明高脂饮食可能通过抑制脂肪酸β氧化导致组织细胞内脂质蓄积,最终造成IR,而用PPAR-α基因的抑制或促进作用,而是作为配体与PPAR-α受体结合对脂肪酸的氧化起调节作用.     

同时激活肝X受体和过氧化物酶体增殖剂激活受体α对大鼠胆汁酸合成的影响

目的 研究肝X受体（LXR）和过氧化物酶体增殖剂激活受体α（PPARα）同时被激活对大鼠胆汁酸合成的影响。方法 雄性SD大鼠分为对照组、血高胆固醇组（HC组）和血高胆固醇＋非诺贝特组（HC＋FENO组）。测定3组大鼠的总胆汁酸水平（血清和粪胆汁酸含量之和）,RT—PCR方法检测肝过氧化物酶体棕榈酰CoA氧化酶（Acox1）、LXR、胆固醇70α-羟化酶（CYP7A1）、D-双功能蛋白（DBP）、三羟基粪甾烷酰CoA氧化酶（Acox2）、固醇12α-羟化酶（CYP8B1）和固醇27-羟化酶（CYP27A1）mRNA的表达水平。结果 HC＋FENO组的总胆汁酸水平显著高于HC组（P〈0．01）,且两组均显著高于对照组（P〈0．01）;对照组和HC组的Acox1和DBPmRNA水平差异无显著性,但均低于HC＋FENO组（P〈0．01）;HC＋FENO组和HC组的LXR和CYP7A1mRNA水平差异无显著性,但均高于对照组（P〈0．01,P〈0．05）;3组的Acox2、CYPSB1和CYP27A1mRNA水平差异均无显著性。结论 同时激活大鼠肝LXR和PPARα可上调CYP7A1和DBPmRNA的表达,通过经典途径增加胆汁酸的合成。     

Astragalus mongholicus and Angelica sinensis compound alleviates nephrotic hyperlipidemia in rats

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LPL基因mRNA在精神分裂症模型大鼠脑组织中的表达

目的: 探讨脂蛋白酯酶(LPL)基因mRNA在精神分裂症模型大鼠前脑皮层、杏仁核、尾壳核和海马4个脑区中的表达,阐明其在精神分裂症发病中的作用机制。 方法: 选择围产期Wistar大鼠,模型组24只,对照组21只,建立苯环已哌啶(PCP)处理的大鼠精神分裂症动物模型,通过Morris水迷宫实验验证动物模型是否建立成功,并检测其认知改变,采用实时荧光定量PCR法检测LPL基因mRNA在精神分裂症模型大鼠前脑皮层、杏仁核、尾壳核和海马4个脑区中的表达。 结果: Morris水迷宫实验,与对照组比较,模型组大鼠找到平台的时间明显延长,为对照组的4.25倍(P<0.01);与对照组比较,模型组大鼠脑组织中前脑皮层和海马区LPL mRNA表达水平降低,分别下降了61.7%和89.0%(P<0.05)。 结论: LPL基因在大鼠前脑皮层和海马表达水平降低可能与精神分裂症有关联,并且可能与认知障碍存在一定的联系。     

非诺贝特及二甲双胍对OLETF大鼠肾损伤和脂质沉积的影响

目的:探讨自发性2型糖尿病的动物模型OLETF大鼠在糖尿病前期时肾脂质代谢异常与早期肾病变的关系,肾脂质代谢异常的分子机制,以及非诺贝特或二甲双胍治疗对肾脂质代谢及肾病变的影响.方法:8周龄雄性OLETF大鼠,随机分为非诺贝特治疗组(OLETF/F)、二甲双胍治疗组(OLETF/M)和未治疗组,LETO大鼠为正常对照组.于17周龄及30周龄时分别杀检,测定24h尿白蛋白定量,肾皮质中甘油三酯的含量,肾皮质固醇调节元件结合蛋白-1(sterol regulatory element-binding protein 1,SREBP-1)的蛋白及mRNA表达,脂肪酸合成酶(fatty acid synthase,FAS)和乙酰辅酶A羧化酶(acetyl CoA carboxylase,ACC)的mRNA表达水平.结果:OLETF大鼠具有肥胖、高血糖、高胰岛素血症、高血脂的特点.30周龄时OLETF大鼠未治疗组与正常对照组比较,24h尿微量白蛋白显著升高,出现肾早期损伤.OLETF大鼠24 h尿白蛋白定量与肾甘油三酯含量呈正相关(r=0.870,P=0.011),随着肾甘油三酯含量加重,24 h尿白蛋白定量增多.OLETF大鼠未治疗组与正常对照组比较,调节脂肪合成的分子SREBP-1蛋白水平、FASmRNA、ACCmRNA分别升高43.2%(P＜0.01),126.0%(P＜0.01),72.3%(P＜0.01).OLETF/F组的SREBP-1蛋白水平、FASmRNA、ACCmRNA分别低于OLETF未治疗组15.7%(P=0.061),36.8%(P＜0.05),40.3%(P＜0.05).OLETF/M组的SREBP-1蛋白水平、FASmRNA、ACCmRNA分别低于OLETF未治疗组19.3%(P＜0.01),57.3%(P＜0.01),22.5%(P＜0.05).SREBP-1的mRNA水平在各组之间比较差异无统计学意义.结论:OLETF大鼠在糖尿病前期已经出现肾病变,可能与肾脂肪沉积有关.肾组织中SREBP-1水平升高,通过调节FAS,ACC等脂肪合成相关的酶,增加肾脂肪沉积,这可能是糖尿病肾病的发生机制之一.早期给予非诺贝特或二甲双胍治疗,可以减轻OLETF大鼠肾早期病变,可能通过SREBP-1及其下游脂肪合成相关酶的变化,直接改善了肾组织中的脂肪沉积.     

基质金属蛋白酶/组织金属蛋白酶抑制物表达失衡在衰老大鼠肾小管间质损害中的意义

目的研究基质金属蛋白酶(MMP)及组织金属蛋白酶抑制物(TIMP)在不同鼠龄的单侧输尿管梗阻(UUO)大鼠肾小管间质中的表达变化,探讨其可能的作用.方法选用3月、26月龄大鼠制备UUO模型,采用组织病理及逆转录-聚合酶链反应(RT-PCR)、Western印迹等方法观察UUO术后3、7、14 d不同鼠龄大鼠的肾脏组织学改变和MMP-2、MMP-9、TIMP-1、TIMP-2等在梗阻肾小管间质中的表达情况;用明胶酶谱法检测UUO术后不同时间点MMP-2、MMP-9的蛋白水解活性.结果在对照组,TIMP-1、TIMP-2仅微弱表达于3月龄肾脏中,而在26月龄大鼠肾脏中其表达显著增加(P<0.01);老年鼠肾组织中MMP-2、MMP-9的蛋白水解活性显著低于3月龄大鼠(P<0.01).与对照组相比,3月龄、26月龄大鼠梗阻侧肾脏的肾小管间质纤维化面积随UUO术后时间的延长而增加,TIMP-1、TIMP-2及MMP-2、MMP-9的mRNA及蛋白质的表达在术后各时间点均显著增高(P<0.01), MMP-2和MMP-9的蛋白水解活性随UUO术后时间的延长而逐渐下降.其活性的下降与TIMP-2及TIMP-1蛋白质表达的增加呈明显的负相关.与3月龄鼠比较,26月龄鼠肾小管间质纤维化面积在UUO术后各时间点也明显增加(P<0.01),TIMP-1、TIMP-2在肾组织中各时间点的mRNA及蛋白质表达均显著增高(P<0.01),MMP-2、MMP-9的蛋白水解活性在各时间点均显著下降(P<0.01).结论衰老引起的TIMP的高表达及MMP蛋白水解活性下降可能是使衰老大鼠肾小管间质损害加重的重要因素之一.     

瘦素在肝缺血/再灌注诱导的肝损伤中的作用

目的 研究瘦素(Leptin)在肝缺血/再灌注(H-I/R)后发生的变化,以及它对H-I/R诱导的肝损伤的影响.方法 建立大鼠70% H-I/R模型,设立假手术和不同再灌注时间的损伤组.采用放射免疫分析法检测损伤后各组血清、脂肪组织瘦素蛋白水平,采用酶比色法检测损伤后血清丙氨酸氨基转移酶,采用HE染色和免疫组织化学法分别检测损伤后肝的病理改变和瘦素蛋白表达,并采用RT-PCR法检测损伤后脂肪组织、肝瘦素mRNA表达.结果 与损伤后假手术组相比,缺血60 min/再灌注360 min(I60'R360')组血清瘦素显著升高,I60'R60'组脂肪组织瘦素蛋白水平显著升高,4个再灌注组血清丙氨酸氨基转移酶均显著升高.病理学观察提示H-I/R早期肝损伤较重而后期逐步减轻.与损伤后假手术组相比,I60'R60'、I60'R240'组肝瘦素蛋白表达显著升高,I60'R150'组脂肪组织瘦素mRNA表达显著降低,I60'R60'组肝瘦素mRNA表达显著升高,I60'R150'、I60'R240'和I60'R360'组肝瘦素mRNA表达均显著降低.结论 瘦素在H-I/R后发生明显的表达变化,它可能作为一种保护因子对抗H-I/R诱导的肝损伤.     

裸鼹鼠外周血白细胞免疫相关因子mRNA表达水平的检测

目的 检测生长期和成年期裸鼹鼠外周血白细胞免疫相关因子mRNA表达水平,以了解裸鼹鼠的正常免疫水平.方法 通过眼眶静脉丛采集6月龄和12月龄裸鼹鼠外周血,提取外周血白细胞mRNA,反转录成cDNA后,实时定量PCR检测各组裸鼹鼠外周血中白细胞IL-1、IL-2、IL-4、IL-6、IL-8、IL-12、TN F-α、IFN-γ的mRNA表达水平.结果 除了IFN-γ、IL-4各组间无显著差异,6月龄裸鼹鼠的IL-2、TNF-α显著高于12月龄裸鼹鼠,尤其是6月龄雄性裸鼹鼠的表达水平显著较高.而细胞因子IL-1,IL-6中,6月龄雄性裸鼹鼠的表达水平也显著高于12月龄裸鼹鼠.另外,对细胞因子IL-8、IL-12表达检测结果表明,12月龄雌性裸鼹鼠的IL-8表达水平最低,而12月龄雄性裸鼹鼠的IL-12表达最低.结论 生长期雄性裸鼹鼠的细胞免疫水平和体液免疫水平均高于同龄的雌性动物和成年动物.