Thymus quinquecostatus Celak. ameliorates cerebral ischemia-reperfusion injury via dual antioxidant actions: Activating Keap1/Nrf2/HO-1 signaling pathway and directly scavenging ROS

Fan, Shusheng; Liu, Xiaoyun; Wang, Yu; Ren, Xueyang; Liu, Yue; Dong, Ying; Fan, Qiqi; Wei, Jing; Ma, Jiamu; Yu, Axiang; Song, Ruolan; Shen, Meng; Fang, Fang; Xia, Qing; She, Gaimei

doi:10.1016/j.phymed.2021.153673

Cited by 30 publications

(15 citation statements)

References 30 publications

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“…18,19 Recently, some researchers have found that natural thyme polyphenols (TP) are mainly composed of scutellarin and rosmarinic acid, and accompanied by small amounts of vanillic acid, chlorogenic acid, and caffeic acid, which have significant roles in improving cerebral ischemia-reperfusion injury and scavenging reactive oxygen species (ROS). 20,21 Surprisingly, rosmarinic acid has a potential effect on alleviating the inflammatory response of DSS-induced colitis. 22 Closely connected with the previous studies mentioned above, since TP has obvious anti-inflammatory and antioxidant activities, it also has an unspecified potential intervention effect on UC.…”

Section: Introductionmentioning

confidence: 99%

Thyme (Thymus vulgaris L.) polyphenols ameliorate DSS-induced ulcerative colitis of mice by mitigating intestinal barrier damage, regulating gut microbiota, and suppressing TLR4/NF-κB-NLRP3 inflammasome pathways

Zhou

Tian

et al. 2023

Food Funct.

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Section: Introductionmentioning

confidence: 99%

Thyme (Thymus vulgaris L.) polyphenols ameliorate DSS-induced ulcerative colitis of mice by mitigating intestinal barrier damage, regulating gut microbiota, and suppressing TLR4/NF-κB-NLRP3 inflammasome pathways

Zhou

Tian

et al. 2023

Food Funct.

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“…Polyphenol-rich fraction (PRF) has an obvious protective effect on cerebral ischemia injury, which is manifested in PRF’s ability to improve the neurological deficit after transient middle cerebral artery occlusion (tMCAO) and to reduce the infarction rate and improve the cell morphology of the hippocampal CA1 area. PRF regulated oxidative stress by regulating the Keap1/Nrf2/HO-1 pathway and exhibited a good protective effect against CIRI [ 105 ]. To summarize, Keap1/Nrf2 signaling pathway is an effective mechanism to regulate brain injury.…”

Section: Activation Of Nrf2 Signaling Pathway In Cerebral Ischemic St...mentioning

confidence: 99%

Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke

et al. 2022

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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.

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“…For the sham operation control group, the monofilament was withdrawn immediately after CBF reduction started. Taking into account the effect of drugs on the functional scores after stroke, mice were not given any painkillers during 24 h reperfusion time (Fan et al, 2021;Jayaraman et al, 2020). The mice recovered within a specified period of time in a 37°C incubator and had free access to food and water.…”

Section: Transient Middle Cerebral Artery Occlusion (Tmcao) Model and Study Designmentioning

confidence: 99%

TBC1Domain Family Member 25 deficiency aggravates cerebral ischemia‐reperfusion injury via TAK1‐JNK/p38 pathway

Zhang

et al. 2021

Journal of Neurochemistry

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TBC1Domain Family Member 25 (TBC1D25) is a protein that contains a TBC/ RAB-GTPase activating protein (GAP) domain, which was shown to participate in autophagy in previous studies. However, the role of TBC1D25 in cerebral ischemiareperfusion (I/R) injury remains unknown. In this study, we found that the mRNA and protein expression levels of TBC1D25 decreased in mouse brain after I/R injury and primary cortical neurons treated with oxygen and glucose deprivation/reoxygenation (OGD/R). Then TBC1D25 knockout (KO) mice were applied to demonstrate that TBC1D25 ablation aggravated cerebral I/R-induced neuronal loss and infarct size. In addition, neuronal apoptosis and inflammation were significantly potentiated in the TBC1D25-KO group. In in vitro OGD/R model, TBC1D25 knockdown can attenuate neuronal cell viability and aggravate the process of inflammation and apoptosis.Conversely, over-expression of TBC1D25 in primary neurons ameliorated the aforementioned processes. Mechanistically, RNA-sequencing (RNA-seq) analysis revealed mitogen-activated protein kinase (MAPK) signaling pathway was the most significant pathway that contributed to TBC1D25-mediated brain I/R injury process. Through experimental verification, TBC1D25 deficiency increased the phosphorylation of the transforming growth factorβ-activated kinase 1 (TAK1)-c-Jun N-terminal kinase (JNK)/p38 axis in neurons during the brain I/R injury. Furthermore, we found that TAK1 blockade abrogated the apoptosis and inflammatory response produced by TBC1D25 knockdown in vitro. In conclusion, this study is the first to demonstrate the functional significance of TBC1D25 in the pathophysiology of brain I/R injury, and the protective mechanism of TBC1D25 is dependent on the TAK1-JNK/p38 pathway.

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Thymus quinquecostatus Celak. ameliorates cerebral ischemia-reperfusion injury via dual antioxidant actions: Activating Keap1/Nrf2/HO-1 signaling pathway and directly scavenging ROS

Cited by 30 publications

References 30 publications

Thyme (Thymus vulgaris L.) polyphenols ameliorate DSS-induced ulcerative colitis of mice by mitigating intestinal barrier damage, regulating gut microbiota, and suppressing TLR4/NF-κB-NLRP3 inflammasome pathways

Thyme (Thymus vulgaris L.) polyphenols ameliorate DSS-induced ulcerative colitis of mice by mitigating intestinal barrier damage, regulating gut microbiota, and suppressing TLR4/NF-κB-NLRP3 inflammasome pathways

Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke

TBC1Domain Family Member 25 deficiency aggravates cerebral ischemia‐reperfusion injury via TAK1‐JNK/p38 pathway

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