本文選題：鋅 + 糖尿病腎病��； 參考：《吉林大學(xué)》2015年博士論文

【摘要】：糖尿病（diabetes mellitus，DM）是由葡萄糖產(chǎn)生和代謝異常導(dǎo)致內(nèi)環(huán)境紊亂而引發(fā)的多因素的慢性代謝障礙性疾病。它的主要特點(diǎn)是由于胰島的產(chǎn)生、分泌異�；蚨呓钥珊鸵葝u素抵抗、炎癥、氧化應(yīng)激等造成的血糖和血脂代謝失衡。隨著經(jīng)濟(jì)的迅猛發(fā)展、生活標(biāo)準(zhǔn)的提高、飲食和生活方式的改變和老齡化，糖尿病已經(jīng)成為世界范圍內(nèi)的重要的公共健康問(wèn)題，是繼惡性腫瘤和心腦血管疾病之后的第三大威脅公共健康的疾病。據(jù)統(tǒng)計(jì)糖尿病的全球患病人數(shù)在2000年已經(jīng)達(dá)到1.51億人，預(yù)計(jì)2030年在年齡大于20歲的人群中患病人數(shù)將達(dá)到5.52億。糖尿病及其并發(fā)癥的治療給個(gè)人、家庭及社會(huì)都帶來(lái)了沉重的經(jīng)濟(jì)負(fù)擔(dān)，如何預(yù)防糖尿病和控制糖尿病并發(fā)癥的發(fā)生發(fā)展，已經(jīng)成為醫(yī)學(xué)界迫于被解決的熱點(diǎn)問(wèn)題。 糖尿病可以影響機(jī)體的多種器官系統(tǒng)，，如腎臟系統(tǒng)、神經(jīng)系統(tǒng)和眼睛等，隨著時(shí)間的進(jìn)展都可以導(dǎo)致嚴(yán)重的糖尿病并發(fā)癥。作為糖尿病微血管疾病之一的糖尿病腎病，不僅是糖尿病最常見(jiàn)的并發(fā)癥之一，也是糖尿病患者死亡的最主要病因之一。盡管控制血糖、血壓、降低脂質(zhì)水平和抑制腎素血管緊張素系統(tǒng)被用于治療糖尿病，但糖尿病腎病的發(fā)生和發(fā)展仍是不可預(yù)防的。糖尿病腎病的主要組織學(xué)特點(diǎn)是腎小球肥大、腎小球基底膜增厚、細(xì)胞外基質(zhì)增多和最終的腎小球球性硬化。而氧化應(yīng)激介導(dǎo)糖尿病對(duì)腎臟組織功能的不利影響；高血糖誘導(dǎo)的活性氧自由基干擾微血管和促進(jìn)細(xì)胞外基質(zhì)積聚。所以，如何調(diào)節(jié)氧化酶活性和提高抗氧化能力被認(rèn)為是預(yù)防和延緩糖尿病腎病的發(fā)生和發(fā)展的重要手段之一。 鋅作為人體的必需微量元素之一，參與多種生理過(guò)程。同時(shí)，鋅是蛋白的必要組成部分，主要參與維持細(xì)胞結(jié)構(gòu)和細(xì)胞膜的穩(wěn)定性。鋅的功能包括可以維持人類基因組中2000多種鋅依賴的轉(zhuǎn)錄因子的細(xì)胞結(jié)構(gòu)穩(wěn)定，并且對(duì)超過(guò)300多種鋅金屬酶的生物活性起著關(guān)鍵作用。 在糖尿病狀態(tài)下，常伴有鋅缺乏。除了飲食過(guò)程中鋅攝入不足，糖尿病患者吸收和/或重吸收鋅受損和尿鋅排泄增加，都可以增加內(nèi)源性鋅的丟失。鋅不僅在胰島素作用和碳水化合物代謝中起著重要的作用，而且在機(jī)體的抗氧化機(jī)制中也有著不可或缺的作用。目前，氧化應(yīng)激已經(jīng)被認(rèn)為在糖尿病及其并發(fā)癥的發(fā)病機(jī)制中至關(guān)重要。鋅是超氧化物歧化酶等關(guān)鍵的抗氧化酶的重要組成部分，鋅缺乏導(dǎo)致抗氧化酶的抗氧化能力下降，從而導(dǎo)致機(jī)體內(nèi)氧化應(yīng)激增加。但是不同含量的鋅對(duì)糖尿病腎病的作用及其可能的具體機(jī)制尚不明確，為此我們進(jìn)行了以下研究。 我們給予8周齡的FVB雄性小鼠小劑量STZ（50mg/kg）連續(xù)腹腔注射5天，1周后通過(guò)小鼠尾靜脈檢測(cè)血糖，以血糖水平大于16.7mmol/L定為成功建立1型糖尿病動(dòng)物模型。成模后，我們給予美國(guó)Research Diets公司的商品化不同含量鋅的成品飼料飼養(yǎng)糖尿病和對(duì)照組小鼠3個(gè)月，通過(guò)體內(nèi)鋅含量檢測(cè)證實(shí)成功建立不同鋅含量的1型糖尿病動(dòng)物模型。然后，我們通過(guò)Western blot，病理組織學(xué)檢查等實(shí)驗(yàn)方法檢測(cè)腎功能、腎臟病理改變、氧化損傷、炎癥損傷和纖維化損傷，探討不同含量的鋅飼養(yǎng)對(duì)糖尿病小鼠誘導(dǎo)腎臟損傷的作用。隨后，我們通過(guò)檢測(cè)Nrf2及其下游抗氧化因子的表達(dá)水平，探討不同含量的鋅對(duì)糖尿病誘導(dǎo)腎臟損傷作用的可能機(jī)制。最后，我們檢測(cè)AKT、GSK-3β及Fyn水平，進(jìn)一步探討鋅對(duì)AKT及其下游相關(guān)代謝信號(hào)的激活作用，從而探討鋅、AKT和Nrf2之間可能的關(guān)系。結(jié)果如下： 1.不同含量的鋅飼養(yǎng)糖尿病小鼠3個(gè)月，糖尿病各組小鼠間的血糖、體重和腎重/體重比值水平差異無(wú)顯著性改變。 2.在糖尿病各組中，低鋅干預(yù)的糖尿病組小鼠的死亡率、ACR值和尿素氮值顯著升高；正常鋅和高鋅干預(yù)可以改善上述癥狀，尤其是高鋅干預(yù)。 3.與其相應(yīng)對(duì)照組比較，糖尿病組中腎臟氧化損傷指標(biāo)SOD1和SOD2的表達(dá)下降，炎癥指標(biāo)PAI-1和TNF-α、纖維化指標(biāo)CTGF和TGF-β1的表達(dá)增加；在糖尿病各組中，低鋅干預(yù)可以使上述損傷進(jìn)一步加重，而正常鋅和高鋅干預(yù)后，尤其是高鋅干預(yù)，可以改善上述腎臟損傷。 4.通過(guò)PAS染色發(fā)現(xiàn)與其相應(yīng)對(duì)照組比較，糖尿病組出現(xiàn)腎小球肥大、細(xì)胞外基質(zhì)增多和腎小管間質(zhì)損傷；通過(guò)透射電鏡檢查發(fā)現(xiàn)與其相應(yīng)對(duì)照組比較，糖尿病組表現(xiàn)為腎小球基底膜增厚、上皮足突節(jié)段融合和腎小管上皮細(xì)胞中線粒體腫脹；低鋅干預(yù)有進(jìn)一步加重上述損傷的趨勢(shì)，而正常鋅和高鋅干預(yù)可以部分改善腎臟的病理?yè)p傷。 5.與其相應(yīng)對(duì)照組比較，糖尿病組腎臟中Nrf2及其下游抗氧化因子的表達(dá)下降；在糖尿病各組中，低鋅干預(yù)可以使其表達(dá)進(jìn)一步下降，而正常鋅和高鋅干預(yù)，可以誘導(dǎo)Nrf2及其下游抗氧化因子的表達(dá)上調(diào)，尤其是高鋅干預(yù)。 6.與其相應(yīng)對(duì)照組比較，糖尿病組腎臟中AKT和GSK-3β的磷酸化水平下降；在糖尿病各組中，低鋅干預(yù)可以使其磷酸化水平進(jìn)一步下降，而正常鋅和高鋅干預(yù)，可以調(diào)節(jié)AKT和GSK-3β的磷酸化水平升高，尤其是高鋅干預(yù)。 7.與其相應(yīng)對(duì)照組比較，糖尿病組腎臟中Fyn核轉(zhuǎn)位增加，導(dǎo)致Nrf2從核內(nèi)轉(zhuǎn)出增加，最終Nrf2降解增加；在糖尿病各組中，低鋅干預(yù)可以使Fyn核轉(zhuǎn)位進(jìn)一步增加，而正常鋅和高鋅干預(yù)，F(xiàn)yn核轉(zhuǎn)位減少，從而上調(diào)Nrf2的表達(dá)，尤其是高鋅干預(yù)。 通過(guò)以上實(shí)驗(yàn)結(jié)果，我們得出結(jié)論：低鋅干預(yù)一定程度上加重了糖尿病誘導(dǎo)的腎臟損傷；而給予正常鋅和高鋅干預(yù)可以對(duì)糖尿病誘導(dǎo)腎臟損傷起到部分的保護(hù)作用，尤其是高鋅干預(yù)；這種保護(hù)作用部分是通過(guò)誘導(dǎo)Nrf2的表達(dá)和功能而實(shí)現(xiàn)的。而可能的調(diào)節(jié)機(jī)制之一是鋅部分通過(guò)活化AKT降低GSK-3β的活性來(lái)抑制Fyn核轉(zhuǎn)位，從而導(dǎo)致Nrf2在細(xì)胞核內(nèi)積聚而增加其下游抗氧化因子NQO1、SOD等的表達(dá)部分實(shí)現(xiàn)其抗氧化損傷的作用，最終對(duì)糖尿病誘導(dǎo)腎臟損傷起到一定程度的保護(hù)作用。
[Abstract]:Diabetes mellitus (DM) is a multi factor chronic metabolic disorder caused by the disturbance of glucose production and metabolism, which is mainly characterized by the production of islets, abnormal secretion of insulin, and the imbalance of blood glucose and lipid metabolism caused by insulin resistance, inflammation, oxidative stress and so on. With the rapid development of economy, the improvement of standard of living, the change of diet and lifestyle and aging, diabetes has become an important public health problem in the world. It is the third major threat to public health after malignant tumor and cardiovascular disease. According to statistics, the number of diabetic global diseases has reached 1. in 2000. 5 billion 100 million people are expected to reach 552 million in the population older than 20 years of age in 2030. The treatment of diabetes and its complications has brought a heavy economic burden to individuals, families and society. How to prevent diabetes and control the development of diabetes complications has become a hot issue in the medical field.
Diabetes can affect a variety of organ systems, such as the kidney system, the nervous system, and the eyes, which can lead to serious diabetic complications as time progresses. As one of the diabetic microvascular diseases, diabetic nephropathy is not only one of the most common complications of diabetes, but also the most important disease of diabetic patients. One of the reasons. Although controlling blood sugar, blood pressure, lowering lipid levels and inhibiting the renin angiotensin system are used in the treatment of diabetes, the occurrence and development of diabetic nephropathy are still not preventable. The main histologic features of diabetic nephropathy are glomerular hypertrophy, thickening of the glomerular basement membrane, increased extracellular matrix and final glomeruli. And oxidative stress mediates the adverse effects of diabetes on the function of the kidneys; hyperglycemia induced reactive oxygen free radicals interferes with microvessels and promotes the accumulation of extracellular matrix. Therefore, how to regulate oxidase activity and increase antioxidant capacity is considered as an important means to prevent and delay the occurrence and development of hyperglycuria nephropathy One of.
Zinc is one of the essential trace elements of the human body and participates in a variety of physiological processes. At the same time, zinc is a necessary component of the protein. It is mainly involved in maintaining the stability of the cell structure and cell membrane. The function of zinc includes the stability of the cell structure of more than 2000 zinc dependent transcription factors in the human genome, and more than 300 kinds of zinc gold. The biological activity of the enzyme plays a key role.
In diabetes, zinc deficiency is often accompanied by deficiency of zinc. In addition to insufficient zinc intake during diet, the loss of endogenous zinc can be increased in diabetic patients with impaired absorption and / or reabsorption of zinc and increased urine zinc excretion. Zinc not only plays an important role in insulin and carbohydrate metabolism, but also in the body's antioxidant mechanism. At present, oxidative stress has been considered important in the pathogenesis of diabetes and its complications. Zinc is an important component of the key antioxidant enzymes such as superoxide dismutase. Zinc deficiency leads to the decline in antioxidant capacity of antioxidant enzymes, resulting in increased oxidative stress in the body. The role of zinc in diabetic nephropathy and its possible mechanism are not clear.
We gave 8 weeks old FVB male mice with small dose STZ (50mg/kg) for 5 days of continuous intraperitoneal injection. After 1 weeks, the blood glucose was detected by the tail vein of mice. The model of type 1 diabetes mellitus was established successfully with the blood glucose level greater than 16.7mmol/L. After 3 months of disease and control mice, the zinc content of type 1 diabetic animal models with different zinc content was successfully established. Then, we examined renal function, pathological changes of kidney, oxidative damage, inflammatory injury and fibrosis by Western blot and histopathological examination. The effect of diabetic mice induced renal injury. Then, by detecting the expression level of Nrf2 and its downstream antioxidant factors, we explored the possible mechanism of different levels of zinc on diabetic induced renal injury. Finally, we detected the levels of AKT, GSK-3 beta and Fyn, and further explored the activation of zinc on AKT and its downstream related metabolic signals. To explore the possible relationship between zinc, AKT and Nrf2. The results are as follows:
1. there was no significant difference in blood sugar, body weight and kidney weight / body weight ratio among diabetic mice in different concentrations of zinc for 3 months.
2. in the diabetic group, the mortality, ACR and urea nitrogen in the low zinc intervention diabetic group increased significantly, and the intervention of normal zinc and high zinc could improve the above symptoms, especially the high zinc intervention.
3. compared with the corresponding control group, the expression of renal oxidative damage index SOD1 and SOD2 decreased in the diabetic group, the expression of inflammatory markers PAI-1 and TNF- a, the expression of CTGF and TGF- beta 1 in the fibrosis index increased. In the diabetic group, the low zinc intervention could further aggravate the above damage, and the prognosis of normal zinc and high zinc, especially the high zinc intervention, could be used in diabetic group. To improve the injury of the kidneys.
4. compared with the corresponding control group, the diabetic group showed the glomerular hypertrophy, the increase of extracellular matrix and the renal tubulointerstitial damage in the diabetic group. Through the transmission electron microscopy, the diabetic group showed the thickening of the glomerular basement membrane, the fusion of the epithelial podocyte segment and the mitochondria in the renal tubular epithelial cells compared with the corresponding control group. Swelling, low zinc intervention further aggravated the above damage trend, while normal zinc and high zinc intervention can partially improve the pathological damage of kidney.
5. compared with the corresponding control group, the expression of Nrf2 and its downstream antioxidant factors in the kidneys of the diabetic group decreased, and the low zinc intervention could further decrease the expression in the diabetic group, while the intervention of normal zinc and high zinc could induce the up regulation of Nrf2 and its downstream antioxidant factors, especially the high zinc intervention.
6. compared with the corresponding control group, the level of phosphorylation of AKT and GSK-3 beta in the kidneys of the diabetic group decreased, and the low zinc intervention could further decrease the phosphorylation level in the diabetic group, while the normal zinc and the high zinc intervention could regulate the increase of the phosphorylation level of AKT and GSK-3 beta, especially the high zinc intervention.
7. compared with the corresponding control group, the Fyn nucleus transposition in the kidneys of the diabetic group increased, resulting in the increase of Nrf2 from the nucleus and the increase of Nrf2 degradation. In all diabetic groups, the low zinc intervention could further increase the transposition of the Fyn nucleus, while the normal zinc and high zinc intervention, the Fyn nuclear transposition decreased, so that the expression of Nrf2 was up-regulated, especially the high zinc intervention.
Through the experimental results, we conclude that low zinc intervention aggravates the renal injury induced by diabetes to some extent, and that the intervention of normal zinc and high zinc can partly protect the kidney injury induced by diabetes, especially the high zinc intervention; this protection is partly by inducing the expression and function of Nrf2. One of the possible regulatory mechanisms is that one of the possible mechanisms of regulation is that the zinc part reduces the GSK-3 beta activity by activating AKT to inhibit the transposition of the Fyn nucleus, resulting in the accumulation of Nrf2 in the nucleus and increasing its downstream antioxidant factor NQO1, SOD and other expressions to achieve its antioxidant damage, which ultimately induces a certain degree of renal injury induced by diabetes. The protective effect.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2015
【分類號(hào)】：R587.2

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