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逆熵官网(www.ipfs8.vip):若是爱因斯坦生前弥补亚腈胺会怎样?

2021-05-15 15:19 杉宝抗朽迈研究

【文献解读】

美国心脏协会杂志(Journal of the American Heart Association)于2020年4月宣布一篇文章,指出实验性腹自动脉瘤模子小鼠弥补亚精胺可以维持其自动脉结构完整性,削弱自动脉炎性浸润,增添自噬相关卵白的表达,抑制实验性腹自动脉瘤的生长。

研究选择C57BL/6J雄性小鼠,通过向自动脉内输注猪胰弹性卵白酶诱发了实验性腹自动脉瘤,随后在饮用水中添加亚精胺举行治疗。效果发现,小鼠在接受亚精胺治疗后血浆中亚精胺水平显著提高,由对照组的4μM/mL增添至6μM/mL。而且,亚精胺的摄入不影响小鼠的摄食量和体重。在腹自动脉瘤生长方面,对照组腹自动脉瘤发病率为100%,亚精胺治疗后发病率降至72.22%,最大自动脉直径由对照组的1.67mm降至1.26mm。进一步组织考察发现,用亚精胺治疗的小鼠动脉弹性卵白损坏和平滑肌细胞耗竭均显著削弱。这些效果解释晰亚精胺对腹自动脉瘤的生长有抑制作用。

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此外,亚精胺治疗可削减自动脉炎症反映,显示在巨噬细胞浸润水平减小和实验性腹自动脉瘤中的循环炎症细胞降低。研究者在网络的临床腹自动脉瘤患者样品中检测到自噬功效失调,而在小鼠中,亚精胺治疗增添了自噬相关卵白的表达,这可能是亚精胺治疗腹自动脉瘤的潜在靶标。

作者指出,亚精胺是一样平常饮食中存在的自然化合物,外源弥补后不太可能发生不良反映,因此在临床中作为腹自动脉瘤的治疗药物可能异常有前途。

【文献节选】

Background

The protective effects of polyamines on cardiovascular disease have been demonstrated in many studies. However, the roles of spermidine, a natural polyamine, in abdominal aortic aneurysm (AAA) disease have not been studied. In this study, we investigated the influence and potential mechanisms of spermidine treatment on experimental AAA disease.

Methods and Results

Experimental AAAs were induced in 8- to 10-week-old male C57BL/6J mice by transient intra-aortic infusion of porcine pancreatic elastase. Spermidine was administered via drinking water at a concentration of 3 mmol/L. Spermidine treatment prevented experimental AAA formation with preservation of medial elastin and smooth muscle cells. In immunostaining, macrophages, T cells, neutrophils, and neovessels were significantly reduced in aorta of spermidine-treated, as compared with vehicle‐treated elastase‐infused mice. Additionally, flow cytometric analysis showed that spermidine treatment reduced aortic leukocyte infiltration and circulating inflammatory cells. Furthermore, we demonstrated that spermidine treatment promoted autophagy‐related proteins in experimental AAAs using Western blot analysis, immunostaining, and transmission electron microscopic examination. Autophagic function was evaluated for human abdominal aneurysmal and nonaneurysmal adjacent aortae from AAA patients using Western blot analysis and immunohistochemistry. Dysregulated autophagic function, as evidenced by increased SQSTM1/p62 protein and phosphorylated mTOR, was found in aneurysmal, as compared with nonaneurysmal, aortic segments.

Conclusions

Our results suggest that spermidine supplementation limits experimental AAA formation associated with preserved aortic structural integrity, attenuated aortic inflammatory infiltration, reduced circulating inflammatory monocytes, and increased autophagy-related proteins. These findings suggest that spermidine may be a promising treatment for AAA disease.

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