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母体阿脲暴露诱导仔鼠腰椎损伤及花生四烯酸的保护作用。

Maternal alloxan exposure induces damage in rat offspring lumbar vertebrae and protective role of arachidonic acid.

机构信息

Department of Human Anatomy and Embryology, Faculty of Medicine, Assiut University, Assiut, Egypt;

出版信息

Rom J Morphol Embryol. 2022 Jan-Mar;63(1):83-97. doi: 10.47162/RJME.63.1.08.

DOI:10.47162/RJME.63.1.08
PMID:36074671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9593121/
Abstract

BACKGROUND

Vertebral abnormalities in offspring of diabetic mothers make major challenges worldwide and were not sufficiently studied before.

AIM

To investigate the effects of alloxan-induced diabetes on rats' lumbar vertebrae, and to assess the potential beneficial impact of arachidonic acid.

MATERIALS AND METHODS

Pregnant rats were randomly equally divided into four groups: control, alloxan-induced diabetes received alloxan injection 150 mg∕kg, alloxan + arachidonic acid group received arachidonic acid 10 μg∕animal then given alloxan injection, and arachidonic acid group received it, until offspring age of three weeks. Six male offspring from each group were included in this study at ages of newborn, three-week-old, two-month-old, and their body measurements were recorded. Lumbar vertebrae and pancreas specimens were examined by light microscopy, morphometry, transmission electron microscopy (TEM), and immunohistochemistry for insulin expression.

RESULTS

In alloxan-induced diabetes newborn, three-week-old, and two-month-old rats, body measurements were significantly declined, histomorphometry of 6th lumbar vertebrae revealed disorganized chondrocytes, with vacuolated cytoplasm, empty lacunae, diminished matrix staining, with areas devoid of cells. TEM showed shrunken reserve and proliferative cells, with irregular nuclei, and damaged mitochondria. In contrast, alloxan + arachidonic acid group had cytoarchitecture of lumbar vertebrae that were like control group. Histomorphometry of pancreas in alloxan-induced diabetes group showed significant reduction in pancreatic islets number and surface area, damaged pancreatic islet cells appeared atrophied with apoptotic nuclei, and very weak insulin immunostaining. Whereas alloxan + arachidonic acid group displayed healthy features of pancreatic islets, which resembled control group, with strong insulin immunostaining.

CONCLUSIONS

Arachidonic acid mitigated alloxan-induced diabetes by its antidiabetic activity.

摘要

背景

糖尿病母亲后代的脊柱异常在全球范围内构成重大挑战,但在此之前研究尚不充分。

目的

研究丙烯醛诱导的糖尿病对大鼠腰椎的影响,并评估花生四烯酸的潜在有益作用。

材料和方法

将妊娠大鼠随机平均分为四组:对照组、丙烯醛诱导的糖尿病组给予 150mg∕kg 丙烯醛注射、丙烯醛+花生四烯酸组给予 10μg∕只动物的花生四烯酸,然后给予丙烯醛注射、花生四烯酸组给予花生四烯酸,直至仔鼠 3 周龄。每组取 6 只雄性仔鼠进行研究,分别于新生、3 周龄、2 月龄时进行检测,记录其身体测量值。通过光镜、形态计量学、透射电镜(TEM)和胰岛素免疫组化检测腰椎和胰腺标本。

结果

在丙烯醛诱导的糖尿病新生、3 周龄和 2 月龄大鼠中,身体测量值显著下降,第 6 腰椎的组织形态计量学显示,软骨细胞排列紊乱,细胞质空泡化,腔隙空虚,基质染色减少,细胞缺失。TEM 显示储备细胞和增殖细胞皱缩,细胞核不规则,线粒体受损。相比之下,丙烯醛+花生四烯酸组的腰椎细胞结构类似于对照组。丙烯醛诱导的糖尿病组的胰腺组织形态计量学显示胰岛数量和表面积显著减少,受损的胰岛细胞出现萎缩,细胞核凋亡,胰岛素免疫染色非常弱。而丙烯醛+花生四烯酸组的胰岛显示出与对照组相似的健康特征,胰岛素免疫染色强。

结论

花生四烯酸通过其抗糖尿病活性减轻丙烯醛诱导的糖尿病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/c57b2ae6ff05/RJME-63-1-83-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/1f4c35918abf/RJME-63-1-83-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/de5ef385efcf/RJME-63-1-83-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/82a1ac45737c/RJME-63-1-83-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/f9446a3a148d/RJME-63-1-83-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/2f555ed9c37d/RJME-63-1-83-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/b0a481821ad8/RJME-63-1-83-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/c57b2ae6ff05/RJME-63-1-83-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/1f4c35918abf/RJME-63-1-83-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/de5ef385efcf/RJME-63-1-83-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/82a1ac45737c/RJME-63-1-83-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/f9446a3a148d/RJME-63-1-83-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/2f555ed9c37d/RJME-63-1-83-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/b0a481821ad8/RJME-63-1-83-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b2d/9593121/c57b2ae6ff05/RJME-63-1-83-fig7.jpg

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