4.5 Article

Chronic high-fat diet consumption exacerbates pyroptosis- and necroptosis-mediated HMGB1 signaling in the brain after ischemia and reperfusion injury

期刊

JOURNAL OF PHYSIOLOGY AND BIOCHEMISTRY
卷 78, 期 4, 页码 833-844

出版社

SPRINGER
DOI: 10.1007/s13105-022-00906-4

关键词

Cerebral ischemia; High-fat diet; Obesity; Pyroptosis; Necroptosis; Neuroinflammation

资金

  1. Functional Food Research Center for Well-Being, Chiang Mai University
  2. Royal Golden Jubilee PhD program [PHD/0104/2561]

向作者/读者索取更多资源

This study aimed to investigate the impact of high-fat diet consumption on ischemic stroke and found that it exacerbates pyroptotic and necroptotic cell death, leading to poor post-stroke outcomes.
Obesity is categorized as a common comorbidity found in people who experience an ischemic stroke. However, the mechanisms to explain this correlation have still not been elucidated fully. Pyroptosis and necroptosis are novel forms of programmed cell death that occur upon intracellular danger signals. The major feature of pyroptosis and necroptosis is damage to the lipid membrane, which consequently results in lytic cell death and allows the release of high mobility group box protein 1 (HMGB1) into the extracellular space. We aimed to investigate the influences of high-fat diet (HFD) consumption on cerebral ischemia and reperfusion (I/R) injury and hypothesized that HFD consumption exacerbated the activation of pyroptosis, necroptosis, and HMGB1 signaling pathways. All rats received normal diet (ND) or HFD for 16 weeks. Subsequently, both groups were divided into either a sham- or an I/R-operated group. Twenty-four hours after the surgery, all rats were evaluated for neurological deficits and then sacrificed. After I/R injury, there were more severe functional deficits and larger brain infarcts in the HFD compared with the ND group. The histological observation revealed an increase in tissue abnormalities in the HFD group, consistent with the massive reduction of intact neurons along the peri-infarct region. Furthermore, cerebral I/R injury dramatically activated the pyroptotic, necroptotic, and HMGB1 signaling pathways in HFD-fed rats compared with ND-fed rats. These findings suggest that chronic HFD consumption worsens ischemic brain pathology and leads to poor post-stroke outcomes by exacerbating pyroptotic and necroptotic cell death.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据