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膳食硝酸盐维持氧化应激和肠道微生物群的内稳态,促进 2 型糖尿病大鼠皮瓣存活。

Dietary nitrate maintains homeostasis of oxidative stress and gut microbiota to promote flap survival in type 2 diabetes mellitus rats.

机构信息

Department of Stomatology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Department of Oral and Maxillofacial-Head and Neck Oncology, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.

出版信息

BMC Endocr Disord. 2024 Sep 10;24(1):184. doi: 10.1186/s12902-024-01691-5.

Abstract

BACKGROUND

Random-pattern skin flaps are commonly used to repair skin tissue defects in surgical tissue reconstruction. However, flap necrosis in the distal area due to ischemia injury is still challenging for its applications in plastic surgery. The complications of diabetes will further increase the risk of infection and necrosis.

METHODS

This study induced type 2 diabetes mellitus (T2DM) rats with a high-fat diet and STZ. The survival rate of the skin flap was observed by adding inorganic sodium nitrate to drinking water. Histology and immunohistochemistry were used to detect the damage to the skin flap. The nitrate content was measured by total nitric oxide and nitrate/nitrite parameter assay. Dihydroethidium and malondialdehyde (MDA) assays were used to value oxidative stress. Rat colon feces were collected for 16s rRNA gene sequence.

RESULTS

Our studies showed that nitrate administration leads to anti-obesity and anti-diabetic effects. Nitrate directly increased the survival area of skin flaps in diabetic rats and mean blood vessel density by enhancing angiogenesis, inhibiting apoptosis, and reducing oxidative stress. The 16s rRNA sequence revealed that nitrate may regulate the homeostasis of the gut microbiota and re-store energy metabolism.

CONCLUSION

Dietary nitrate has been shown to maintain the homeostasis of oxidative stress and gut microbiota to promote flap survival in rats with T2DM.

摘要

背景

随意皮瓣常用于外科组织重建中修复皮肤组织缺损。然而,由于缺血损伤导致皮瓣远端坏死,其在整形外科学中的应用仍具有挑战性。糖尿病的并发症会进一步增加感染和坏死的风险。

方法

本研究通过高脂肪饮食和 STZ 诱导 2 型糖尿病(T2DM)大鼠。通过在饮用水中添加无机硝酸钠来观察皮瓣的存活率。组织学和免疫组织化学用于检测皮瓣损伤。通过总一氧化氮和硝酸盐/亚硝酸盐参数测定来测量硝酸盐含量。二氢乙啶和丙二醛(MDA)测定用于评估氧化应激。收集大鼠结肠粪便进行 16s rRNA 基因序列分析。

结果

我们的研究表明,硝酸盐给药具有抗肥胖和抗糖尿病作用。硝酸盐通过增强血管生成、抑制细胞凋亡和减少氧化应激,直接增加糖尿病大鼠皮瓣的存活面积和平均血管密度。16s rRNA 序列显示,硝酸盐可能调节肠道微生物组的内稳态并恢复能量代谢。

结论

饮食硝酸盐已被证明可维持氧化应激和肠道微生物组的内稳态,从而促进 T2DM 大鼠皮瓣的存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/445b/11386097/929bf25ddf56/12902_2024_1691_Fig1_HTML.jpg

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