Glutamine inhibits inflammation, oxidative stress, and apoptosis and ameliorates hyperoxic lung injury.

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of physiology and biochemistry Pub Date : 2023-08-01 DOI:10.1007/s13105-023-00961-5
Shujian Zhang, Xuewei Li, Tiezheng Yuan, Xiangyu Guo, Can Jin, Zhengyong Jin, Jinliang Li
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Abstract

Glutamine (Gln) is the most widely acting and abundant amino acid in the body and has anti-inflammatory properties, regulates body metabolism, and improves immune function. However, the mechanism of Gln's effect on hyperoxic lung injury in neonatal rats is unclear. Therefore, this work focused on examining Gln's function in lung injury of newborn rats mediated by hyperoxia and the underlying mechanism. We examined body mass and ratio of wet-to-dry lung tissue weights of neonatal rats. Hematoxylin and eosin (HE) staining was performed to examine histopathological alterations of lung tissues. In addition, enzyme-linked immunoassay (ELISA) was conducted to measure pro-inflammatory cytokine levels within bronchoalveolar lavage fluid (BALF). Apoptosis of lung tissues was observed using TUNEL assay. Western blotting was performed for detecting endoplasmic reticulum stress (ERS)-associated protein levels. The results showed that Gln promoted body weight gain, significantly reduced pathological damage and oxidative stress in lung tissue, and improved lung function in neonatal rats. Gln reduced pro-inflammatory cytokine release as well as inflammatory cell production in BALF and inhibited apoptosis in lung tissue cells. Furthermore, we found that Gln could downregulate ERS-associated protein levels (GRP78, Caspase-12, CHOP) and inhibit c-Jun N-terminal kinase (JNK) and inositol-requiring enzyme 1 alpha (IRE1α) phosphorylation. These results in an animal model of bronchopulmonary dysplasia (BPD) suggest that Gln may have a therapeutic effect on BPD by reducing lung inflammation, oxidative stress, and apoptosis and improving lung function; its mechanism of action may be related to the inhibition of the IRE1α/JNK pathway.

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谷氨酰胺抑制炎症、氧化应激和细胞凋亡,改善高氧性肺损伤。
谷氨酰胺(Gln)是体内作用最广泛、含量最多的氨基酸,具有抗炎、调节机体代谢、提高免疫功能等作用。然而,Gln对新生大鼠高氧性肺损伤的作用机制尚不清楚。因此,本研究旨在探讨Gln在新生儿高氧大鼠肺损伤中的作用及其机制。我们检测了新生大鼠的体重和干肺组织重量比。采用苏木精和伊红(HE)染色观察肺组织的病理改变。此外,采用酶联免疫分析法(ELISA)测定支气管肺泡灌洗液(BALF)中促炎细胞因子水平。TUNEL法观察肺组织凋亡。Western blotting检测内质网应激(ERS)相关蛋白水平。结果表明,谷氨酰胺促进新生大鼠体重增加,显著减轻肺组织病理损伤和氧化应激,改善肺功能。Gln减少促炎细胞因子的释放和BALF中炎症细胞的产生,抑制肺组织细胞的凋亡。此外,我们发现Gln可以下调ers相关蛋白(GRP78、Caspase-12、CHOP)水平,抑制c-Jun n -末端激酶(JNK)和肌醇要求酶1α (IRE1α)磷酸化。这些结果在支气管肺发育不良(BPD)动物模型中表明,Gln可能通过减少肺部炎症、氧化应激和细胞凋亡以及改善肺功能来治疗BPD;其作用机制可能与抑制IRE1α/JNK通路有关。
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来源期刊
Journal of physiology and biochemistry
Journal of physiology and biochemistry 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
86
审稿时长
6-12 weeks
期刊介绍: The Journal of Physiology and Biochemistry publishes original research articles and reviews describing relevant new observations on molecular, biochemical and cellular mechanisms involved in human physiology. All areas of the physiology are covered. Special emphasis is placed on the integration of those levels in the whole-organism. The Journal of Physiology and Biochemistry also welcomes articles on molecular nutrition and metabolism studies, and works related to the genomic or proteomic bases of the physiological functions. Descriptive manuscripts about physiological/biochemical processes or clinical manuscripts will not be considered. The journal will not accept manuscripts testing effects of animal or plant extracts.
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