Green Tea Polyphenols Modulated Cerebral SOD Expression and Endoplasmic Reticulum Stress in Cardiac Arrest/Cardiopulmonary Resuscitation Rats

Hu, Wanxiang; Qin, Shu; Chen, Menghua; Xie, Lu

doi:10.1155/2020/5080832

Cited by 10 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, reperfusion processes after ischemic attack may further exacerbate brain damage, which is named cerebral ischemia/reperfusion (I/R) injury [5,6]. It is increasingly understood that multiple pathophysiological processes, includ-ing oxidative stress, the inflammatory response, neuronal death, and apoptosis, play a pivotal role in the development of cerebral I/R injury [7][8][9][10]. Thus, treatments based on the above mechanisms are proposed as a promising strategy to attenuate the outcomes of stroke and cerebral I/R injury.…”

Section: Introductionmentioning

confidence: 99%

Palmatine Protects against Cerebral Ischemia/Reperfusion Injury by Activation of the AMPK/Nrf2 Pathway

Tang

Hong

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Palmatine (PAL), a natural isoquinoline alkaloid, possesses extensive biological and pharmaceutical activities, including antioxidative stress, anti-inflammatory, antitumor, neuroprotective, and gastroprotective activities. However, it is unknown whether PAL has a protective effect against ischemic stroke and cerebral ischemia/reperfusion (I/R) injury. In the present study, a transient middle cerebral artery occlusion (MCAO) mouse model was used to mimic ischemic stroke and cerebral I/R injury in mice. Our study demonstrated that PAL treatment ameliorated cerebral I/R injury by decreasing infarct volume, neurological scores, and brain water content. PAL administration attenuated oxidative stress, the inflammatory response, and neuronal apoptosis in mice after cerebral I/R injury. In addition, PAL treatment also decreases hypoxia and reperfusion- (H/R-) induced neuronal injury by reducing oxidative stress, the inflammatory response, and neuronal apoptosis. Moreover, the neuroprotective effects of PAL were associated with the activation of the AMP-activated protein kinase (AMPK)/nuclear factor E2-related factor 2 (Nrf2) pathway, and Nrf2 knockdown offsets PAL-mediated antioxidative stress and anti-inflammatory effects. Therefore, our results suggest that PAL may be a novel treatment strategy for ischemic stroke and cerebral I/R injury.

show abstract

Section: Introductionmentioning

confidence: 99%

Palmatine Protects against Cerebral Ischemia/Reperfusion Injury by Activation of the AMPK/Nrf2 Pathway

Tang

Hong

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Accumulating literatures report that some agents with antioxidant properties have a neuroprotective role against ischemic stroke [ 11 – 13 ]. Similarly, our previous study indicated that antioxidative therapy exerted an effective role against CIRI in CA/CPR rat model [ 14 ]. Some studies on components of citric fruits support the antioxidant, anti-inflammatory, and antinecroptosis effects in several experimental models.…”

Section: Discussionmentioning

confidence: 64%

Pomelo Peel Essential Oil Ameliorates Cerebral Ischemia-Reperfusion Injury through Regulating Redox Homeostasis in Rats and SH-SY5Y Cells

Chen

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

Background. In cardiac accident/cardiopulmonary resuscitation (CA/CPR) rat model, oxidative stress occurs during cerebral ischemia/reperfusion injury (CIRI), and antioxidative treatment has a neuroprotective effect. The antioxidant capabilities of pomelo peel essential oil (PPEO) have mostly been investigated in vitro, with little convincing data in vivo, particularly whether PPEO has a neuroprotective role against CIRI. Methods. In this investigation, a CA/CPR SD rat model and an oxygen-glucose deprivation/reperfusion (OGD/R) SH-SY5Y cell model were used to imitate the CIRI, and the neuroprotective role of PPEO was discovered in both. The morphological changes of neurons after PPEO treatment were observed using Nissl staining and transmission electron microscopy, while biochemical markers such as MDA, GSH, and Fe2+ were evaluated. Furthermore, western blot, immunofluorescence, and immunohistochemistry were used to examine the proteins GPX4, SLC7A11, ACSL4, and Nrf2. Results. Significant morphological alterations were identified during the pathological progression of CIRI. The neurologic deficit scores improved after PPEO therapy, and the expression of GPX4 and SLC7A11 increased, while the levels of intracellular Fe2+, ROS, and ACSL4 declined. PPEO also prevented CIRI caused by erastin (a specific inhibitor of SLC7A11) or RSL3 (inhibitor of GPX4). Furthermore, PPEO-induced increases in SLC7A11 and GPX4 may be related to Nrf2 translocation to the nucleus. Conclusions. In vitro and in vivo, we verified and investigated the neuroprotective effects of PPEO on CIRI. The underlying process may be connected to redox homeostasis regulation, which enhances antioxidative capacity through upmodulation of SLC7A11 and GPX4. It implies that PPEO will be considered as a source of potential adjuvant therapeutic agents for improving CIRI outcomes.

show abstract

“…However, prolonged ERS triggers apoptosis, not directly, but by activating downstream proapoptotic molecules that push cells toward the death pathway. The expression of CHOP is of great significance in inducing prosurvival to proapoptosis [ 39 ]. PERK/eIF2 α /ATF4 pathway is the leading pathway for activation of CHOP among the three branches of UPR.…”

Section: Discussionmentioning

confidence: 99%

Atractylenolide III Attenuates Apoptosis in H9c2 Cells by Inhibiting Endoplasmic Reticulum Stress through the GRP78/PERK/CHOP Signaling Pathway

Zuo

Tang

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

The objective of this study was to determine the effect of atractylenolide III (ATL-III) on endoplasmic reticulum stress (ERS) injury, H9c2 cardiomyocyte apoptosis induced by tunicamycin (TM), and the GRP78/PERK/CHOP signaling pathway. Molecular docking was applied to predict the binding affinity of ATL-III to the key proteins GRP78, PERK, IREα, and ATF6 in ERS. Then, in vitro experiments were used to verify the molecular docking results. ERS injury model of H9c2 cells was established by TM. Cell viability was detected by MTT assay, and apoptosis was detected by Hoechst/PI double staining and flow cytometry. Protein expression levels of GRP78, PERK, eIF2α, ATF4, CHOP, Bax, Bcl-2, and Caspase-3 were detected by Western blot. And mRNA levels of GRP78, CHOP, PERK, eIF2α, and ATF4 were detected by RT-qPCR. Moreover, the mechanism was further studied by using GRP78 inhibitor (4-phenylbutyric acid, 4-PBA), and PERK inhibitor (GSK2656157). The results showed that ATL-III had a good binding affinity with GRP78, and the best binding affinity was with PERK. ATL-III increased the viability of H9c2 cells, decreased the apoptosis rate, downregulated Bax and Caspase-3, and increased Bcl-2 compared with the model group. Moreover, ATL-III downregulated the protein and mRNA levels of GRP78, CHOP, PERK, eIF2α, and ATF4, consistent with the inhibition of 4-PBA. ATL-III also decreased the expression levels of PERK, eIF2α, ATF4, CHOP, Bax, and Caspase-3, while increasing the expression of Bcl-2, which is consistent with GSK2656157. Taken together, ATL-III could inhibit TM-induced ERS injury and H9c2 cardiomyocyte apoptosis by regulating the GRP78/PERK/CHOP signaling pathway and has myocardial protection.

show abstract

Green Tea Polyphenols Modulated Cerebral SOD Expression and Endoplasmic Reticulum Stress in Cardiac Arrest/Cardiopulmonary Resuscitation Rats

Cited by 10 publications

References 33 publications

Palmatine Protects against Cerebral Ischemia/Reperfusion Injury by Activation of the AMPK/Nrf2 Pathway

Palmatine Protects against Cerebral Ischemia/Reperfusion Injury by Activation of the AMPK/Nrf2 Pathway

Pomelo Peel Essential Oil Ameliorates Cerebral Ischemia-Reperfusion Injury through Regulating Redox Homeostasis in Rats and SH-SY5Y Cells

Atractylenolide III Attenuates Apoptosis in H9c2 Cells by Inhibiting Endoplasmic Reticulum Stress through the GRP78/PERK/CHOP Signaling Pathway

Contact Info

Product

Resources

About