慢性不可预知温和应激通过HMGB1/TLR4下调PPARγ/LXRα/ABCA1促进ApoE -/- 小鼠的As病变
发布时间：2020-12-09 23:35
【研究背景与目的】动脉粥样硬化（atherosclerosis,As）是心脑血管疾病的主要病理基础,近年来,由As所致的冠心病、脑卒中、心肌梗死等心脑血管疾病严重危害着人类的身心健康和生活质量,已成为严重的社会问题。研究表明,慢性应激已成为As性心血管疾病的重要独立危险因素。因此,阐明慢性应激影响As病变的分子机制,对As的防治具有重要的意义。在本研究中,我们将探讨高迁移率族蛋白B1（High mobility group box 1,HMGB1）/Toll样受体4（Toll-like receptor 4,TLR4）途径在慢性应激促进As病变中的作用及其机制。【方法】60只ApoE-/-雄性小鼠随机分为4组:对照组、慢性应激组、慢性应激+丙酮酸乙酯（HMGB1抑制剂）组、慢性应激+TAK242（TLR4抑制剂）组。首先,通过检测血清皮质酮水平确定小鼠应激模型是否建立。采用Elisa和Western Blot,检测慢性应激ApoE-/-小鼠As模型血清中HMGB1的释放含量和血管组织中HMGB1和TLR4的表达变化,以明确慢性应激对HMGB1...
【文章来源】：南华大学湖南省
【文章页数】：81 页
【学位级别】：硕士
【部分图文】：
EP或TAK242对CUMSApoE-/-小鼠血清皮质酮水平的影响
2 EP 或 TAK242 对 CUMSApoE-/-小鼠血清 HMGB1 水平 of EP and TAK-242 treatment on serum HMGB1 proteE-/-mice were injected with PBS, EP (50 mg/kg, once dailk) for consecutive 16 weeks by intraperitoneal injection 30 miriod treatment, blood samples were collected for assessment vels in serum were measured by ELISA. Data were expressedalysis was performed by One-Way analysis of variance. *P 0GB1/TLR4 途径可减弱 CUMS 加重的 ApoEMS 促进 ApoE-/-小鼠 HMGB1 释放的基础上，我们随性应激促进 ApoE-/-小鼠的 As 病变中作用及其机制剂 EP（50 mg/kg/d，腹腔注射）和 TLR4 抑制剂 TA-/--/-
图 3.3 EP 或 TAK242 对 CUMSApoE-/-小鼠 As 病变的影响Figure 3.3 Effect of EP and TAK-242 treatment on atherosclerotic lesions in CUMS ApoE-/-mice.Male ApoE-/-mice were injected with PBS, EP (50 mg/kg, once daily), or TAK-242 (0.3 mg/kg, twicea week) for consecutive 16 weeks by intraperitoneal injection 30 minutes prior to CUMS. Over a16-week period treatment, entire aorta from the aortic root to the iliac bifurcation was harvested foranalysis of atherosclerotic lesions. (A) Representative images of H&E, ORO (Oil Red O, ORO), andMasson staining of aortic sinuses. (B) Quantification of atherosclerotic plaque areas of aortic sinusesrevealed that EP or TAK-242 treatment significantly decreased atherosclerotic lesions induced byCUMS (n = 15). (C) Quantification of collagen fibers content of aortic sinuses (n = 15). (D)Representative images of ORO staining of en face aortic atherosclerotic lesions. (E) Quantification ofatherosclerotic lesion areas of aorta was performed by using Image Pro Plus (n = 5). Data wereexpressed as mean ± S.E.M. Statistical analysis was performed by One-Way analysis of variance. *P 0.01, **P 0.01, ***P 0.001.
本文编号：2907664
【文章来源】：南华大学湖南省
【文章页数】：81 页
【学位级别】：硕士
【部分图文】：
EP或TAK242对CUMSApoE-/-小鼠血清皮质酮水平的影响
2 EP 或 TAK242 对 CUMSApoE-/-小鼠血清 HMGB1 水平 of EP and TAK-242 treatment on serum HMGB1 proteE-/-mice were injected with PBS, EP (50 mg/kg, once dailk) for consecutive 16 weeks by intraperitoneal injection 30 miriod treatment, blood samples were collected for assessment vels in serum were measured by ELISA. Data were expressedalysis was performed by One-Way analysis of variance. *P 0GB1/TLR4 途径可减弱 CUMS 加重的 ApoEMS 促进 ApoE-/-小鼠 HMGB1 释放的基础上，我们随性应激促进 ApoE-/-小鼠的 As 病变中作用及其机制剂 EP（50 mg/kg/d，腹腔注射）和 TLR4 抑制剂 TA-/--/-
图 3.3 EP 或 TAK242 对 CUMSApoE-/-小鼠 As 病变的影响Figure 3.3 Effect of EP and TAK-242 treatment on atherosclerotic lesions in CUMS ApoE-/-mice.Male ApoE-/-mice were injected with PBS, EP (50 mg/kg, once daily), or TAK-242 (0.3 mg/kg, twicea week) for consecutive 16 weeks by intraperitoneal injection 30 minutes prior to CUMS. Over a16-week period treatment, entire aorta from the aortic root to the iliac bifurcation was harvested foranalysis of atherosclerotic lesions. (A) Representative images of H&E, ORO (Oil Red O, ORO), andMasson staining of aortic sinuses. (B) Quantification of atherosclerotic plaque areas of aortic sinusesrevealed that EP or TAK-242 treatment significantly decreased atherosclerotic lesions induced byCUMS (n = 15). (C) Quantification of collagen fibers content of aortic sinuses (n = 15). (D)Representative images of ORO staining of en face aortic atherosclerotic lesions. (E) Quantification ofatherosclerotic lesion areas of aorta was performed by using Image Pro Plus (n = 5). Data wereexpressed as mean ± S.E.M. Statistical analysis was performed by One-Way analysis of variance. *P 0.01, **P 0.01, ***P 0.001.
本文编号：2907664
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