Neuroprotection of Resveratrol Against Focal Cerebral Ischemia/Reperfusion Injury in Mice Through a Mechanism Targeting Gut-Brain Axis

Dou, Zhongci; Rong, Xiongfei; Zhao, Erxian; Zhang, Lixia; Lv, Yunqi

doi:10.1007/s10571-019-00687-3

Cited by 82 publications

(68 citation statements)

References 35 publications

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“…We wondered whether CDDO-Me could alter the mouse BBB permeability, which might be related with compound crossing BBB. By utilizing Evans blue (EB) labeling, we tested blood-brain-barrier (BBB) intactness [25,26]. The staining intensity revealed that the mouse brains of different experimental groups failed to be stained by EB (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…We wondered at the first time whether CDDO-Me could alter the mouse BBB permeability, which might be related with compound crossing BBB. Thus, we performed an experiment to estimate BBB permeability by utilizing the Evans blue (EB) labeling method, which is the most common dye in evaluating the BBB integrity [25,26]. The result showed a negative outcome, suggesting that the BBB intactness was not impacted by CDDO-Me.…”

Section: Discussionmentioning

confidence: 99%

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Treatment of obesity-related inflammation with a novel synthetic pentacyclic oleanane triterpenoids via modulation of macrophage polarization

et al. 2019

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Background: Obesity leads to the chronic inflammation in the whole body and triggers the macrophage polarization to the pro-inflammatory phenotype. Targeting macrophage polarization provides a promising therapeutic strategy for obesity-related metabolic disorders and inflammation. Here, we show that SO1989, a derivative of natural occurring compound oleanolic acid, restores the balance between M1-polarized and M2-polarized macrophages in high fat diets (HFD)-induced obese mice resulting in the improvement of adipose inflammation and the metabolic dysfunctions. Methods: Histological analysis, magnetic cell sorting and FACS, in vitro cell model of adipose inflammation, Western blotting, HFD mice model. Findings: SO1989 exhibits similar or even stronger activity in inhibiting inflammation and M1 polarization of macrophages both in vitro and in vivo compared to its analogue CDDO-Me, previously known as a powerful anti-inflammation chemical small molecule. In addition, SO1989 can significantly increase the level of fatty acid oxidation in macrophages which can efficiently facilitate M2 polarization of macrophages. Unlike CDDO-Me, SO1989 shows less adverse effects on obese mice. Interpretation: Taken all together, our findings identify SO1989 as a modulator in macrophage polarization and a safer potential leading compound for pro-resolution of inflammation treatment in metabolic disorders.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Treatment of obesity-related inflammation with a novel synthetic pentacyclic oleanane triterpenoids via modulation of macrophage polarization

et al. 2019

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“…In a mouse model of CIRI, it was demonstrated that a purpura extract can significantly reduce infarct size, restore the activities of antioxidants such as SOD and GSH, and decrease pro-oxidase enzyme activity by xanthine oxidase (Bora and Sharma, 2011). The protective effect of resveratrol on CIRI in mice is also related to its antioxidant properties (Dou et al, 2019). Flavonoids, presented broadly in plants and diets, have also been shown the effect and function on CIRI and cognition in experimental studies on their different flavonoid species, such as quercetine and catechin (Calis et al, 2019).…”

Section: Natural Antioxidantsmentioning

confidence: 99%

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

Xiong

et al. 2020

Front. Mol. Neurosci.

258

197

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The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply. Cerebral ischemia/reperfusion injury (CIRI) often causes irreversible brain damage and neuronal injury and death, which involves many complex pathological processes including oxidative stress, amino acid toxicity, the release of endogenous substances, inflammation and apoptosis. Oxidative stress and inflammation are interactive and play critical roles in ischemia/reperfusion injury in the brain. Oxidative stress is important in the pathological process of ischemic stroke and is critical for the cascade development of ischemic injury. Oxidative stress is caused by reactive oxygen species (ROS) during cerebral ischemia and is more likely to lead to cell death and ultimately brain death after reperfusion. During reperfusion especially, superoxide anion free radicals, hydroxyl free radicals, and nitric oxide (NO) are produced, which can cause lipid peroxidation, inflammation and cell apoptosis. Inflammation alters the balance between pro-inflammatory and anti-inflammatory factors in cerebral ischemic injury. Inflammatory factors can therefore stimulate or exacerbate inflammation and aggravate ischemic injury. Neuroprotective therapies for various stages of the cerebral ischemia cascade response have received widespread attention. At present, neuroprotective drugs mainly include free radical scavengers, anti-inflammatory agents, and anti-apoptotic agents. However, the molecular mechanisms of the interaction between oxidative stress and inflammation, and their interplay with different types of programmed cell death in ischemia/reperfusion injury are unclear. The development of a suitable method for combination therapy has become a hot topic.

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“…The microbiomegut-brain axis plays a role in either ischemic CVD or depression. It has been reported that after stroke, intestinal dysbiosis not only alters the immune balance of the small intestine with an increase in regulatory T cells and a reduction in interleukin-(IL-) 17-positive γδ T cells but also suppresses trafficking of effector T cells from the gut to the leptomeninges [132,133]. In the myocardial infarction model after three-week arterial occlusion, rats began to exhibit depression-like symptoms with increased gastric retention rates [134].…”

Section: Microbiome-gut-brainmentioning

confidence: 99%

The Role of Oxidative Stress in Common Risk Factors and Mechanisms of Cardio-Cerebrovascular Ischemia and Depression

Lin

Wang

Yan

et al. 2019

Oxidative Medicine and Cellular Longevity

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The public health sector faces a huge challenge as a result of the high prevalence and burden of disability caused by ischemic cardio-cerebrovascular disease (CVD) and depression. Although studies have explored the underlying mechanisms and potential therapies to address conditions, there is no treatment breakthrough, especially for depression which is highly influenced by social stressors. However, accumulating evidence reveals that CVD and depression are correlated and share common risk factors, particularly obesity, diabetes, and hypertension. They also share common mechanisms, including oxidative stress (OS), inflammation and immune response, cell death signaling pathway, and microbiome-gut-brain axis. This review summarizes the relationship between ischemic CVD and depression and describes the interactions among common risk factors and mechanisms for these two diseases. In addition, we propose that OS mediates the crosstalk between these diseases. We also reveal the potential of antioxidants to ameliorate OS-related injuries.

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Neuroprotection of Resveratrol Against Focal Cerebral Ischemia/Reperfusion Injury in Mice Through a Mechanism Targeting Gut-Brain Axis

Cited by 82 publications

References 35 publications

Treatment of obesity-related inflammation with a novel synthetic pentacyclic oleanane triterpenoids via modulation of macrophage polarization

Treatment of obesity-related inflammation with a novel synthetic pentacyclic oleanane triterpenoids via modulation of macrophage polarization

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

The Role of Oxidative Stress in Common Risk Factors and Mechanisms of Cardio-Cerebrovascular Ischemia and Depression

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