Rhein protects against cerebral ischemic‑/reperfusion‑induced oxidative stress and apoptosis in rats

Zhao, Qipeng; Wang, Xiaobo; Chen, Ailing; Cheng, Xian; Zhang, Guoxin; Sun, Jianmin; Zhao, Yunsheng; Huang, Yu; Zhu, Yu

doi:10.3892/ijmm.2018.3488

Cited by 37 publications

(42 citation statements)

References 63 publications

(59 reference statements)

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“…The recovery of motor function is often determined by nerve repair after SCI . Rhubarb has effects against cerebral ischemia injury, can alleviate brain tissue injury after ischemia‐reperfusion, and has a protective effect on nervous system injury caused by cerebral ischemia‐reperfusion . Rhein is one of the effective components of rhubarb, and its protective effects on cerebrovascular conditions and tumors have been reported .…”

Section: Resultsmentioning

confidence: 99%

“…26 Rhubarb has effects against cerebral ischemia injury, can alleviate brain tissue injury after ischemia-reperfusion, and has a protective effect on nervous system injury caused by cerebral ischemia-reperfusion. 27,28 Rhein is one of the effective components of rhubarb, and its protective effects on cerebrovascular conditions and tumors have been reported. 29,30 RHL is a new compound produced by the reaction of lysine and rhein, which can dissolve in water and is convenient for drug administration.…”

Section: Discussionmentioning

confidence: 99%

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Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Hao

Wang

Daiping

et al. 2019

The Kaohsiung J of Med Scie

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The current study aims to investigate the effect of rhein lysinate (RHL) on neuromotor function in rats with spinal cord injury (SCI) and to explore the underlying mechanism. A total of 63 adult male SD rats were randomly divided into the sham group, SCI group and RHL group (SCI‐RHL group), with 21 rats in each group. Basso Beattie Bresnahan (BBB) scoring and the inclined plate test were used to evaluate the changes in motor function after SCI. Then, superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and malondialdehyde (MDA) contents were quantified. Caspase‐3‐positive cells in spinal cord tissue were detected by immunohistochemical (IHC) staining, and protein expression was detected by Western blots. Here, our data showed that compared with the SCI group, the BBB score and inclined plate test score of the SCI‐RHL group were significantly higher than those of the SCI group 7 days after the RHL intervention. After 7 days of RHL treatment, the activities of SOD and GSH‐Px in the spinal cord increased significantly. At the same time, RHL reduced the MDA content in spinal cord tissue of SCI rats. Moreover, cleaved‐caspase‐3‐positive cells and apoptotic cells were significantly lower in the SCI‐RHL group than in the SCI group. More importantly, p38 mitogen‐activated protein kinase (p38 MAPK) was significantly decreased in the SCI‐RHL group compared with the SCI group. In summary, RHL can inhibit the activation of the p38 MAPK pathway after SCI, thereby reducing the apoptosis of spinal cord neurons and improving the neuromotor function of SCI rats.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Hao

Wang

Daiping

et al. 2019

The Kaohsiung J of Med Scie

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“…When the AGmex doses had been optimized, mice were post-treated with AGmex or nimodipine (ND) to compare their neuroprotective efficacies. ND was used as the reference agent as it has been used as a positive control in previous studies [10,11].…”

Section: Experimental Schedule For Dosing and Transient Middle Cerebrmentioning

confidence: 99%

“…In the post-tMCAO treatment group, 1,000 mg/kg AGmex was administered 1 h after the end of the tMCAO. The dose of ND was 60 mg/kg bw based on the dose used in previous studies [10,11]. A schematic procedure of the experiment is shown in Fig.…”

Section: Experimental Schedule For Dosing and Transient Middle Cerebrmentioning

confidence: 99%

Root of Angelica gigas Nakai ameliorates ischemic stroke-induced brain injury in mice through the activation of the PI3K/AKT/mTOR and MAPK pathways

Lee¹,

Lim²,

Cho³

2020

Preprint

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Background: Ischemic stroke results in disability and increased risk of morbidity, resulting in a massive burden on patients and caregivers. Recombinant tissue plasminogen activator (r-tPA) has a limited window of opportunity for efficacy and causes side effects including hemorrhage; therefore, safer and more effective therapeutic strategies are required. In this study, the neuroprotective effects of a methanolic extract of AGR (AGmex) in ischemia/reperfusion-induced brain injury in mice were investigated. Methods: Ischemic brain injury was induced in the mice by transient occlusion of the middle cerebral artery (tMCAO) for 120 min, and the effect of AGmex on the amount of infarction was measured. Cresyl violet and hematoxylin and eosin stains were used to identify changes in the neurons, nuclei, and cytoplasm. Western blotting, immunohistochemistry, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining were used to elucidate the neuroprotective mechanism of AGmex. Results: AGmex effectively reduced the infarction volume when the mice were pre-treated at 1,000 mg/kg bw/day for two consecutive days (AGmex 1000 group). Neurons, nuclei, and cytoplasmic staining were the lowest in the MCAO group, but recovered in the AGmex 1000 group. In addition, proteins related to cell growth, differentiation, and death were up-regulated in the AGmex 1000 group. Conclusion: The major recovery mechanisms appeared to be attenuation of the mitochondrial function of Bcl-2/Bax, and activation of the PI3K/AKT/mTOR and MAPK signaling pathways in ischemic neurons.

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“…Since reperfusion is still the main treatment method to rescue infraction for myocardial ischemic infarction patients, the ischemic/reperfusion (I/R) injury is still clinical challenge (1)(2)(3). Many molecular mechanisms and signaling pathways are involved during the I/R process, including activation of cell apoptosis pathways (4), induction of mitochondrial damage (5) and ATP dysfunction (6) and also the increase of oxidative stress (7).…”

Section: Introductionmentioning

confidence: 99%

CFTR improves myocardial ischemic/reperfusion injury through activating FUNDC1-mediated mitophagy and regulating ATP and mitochondrial functions

Zhang¹,

Ding²,

Yi³

et al. 2020

Preprint

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Background To investigate the potential role of CFTR in myocardial ischemic/reperfusion (I/R) injury and its relationship with mitophagy. Methods Wild type (WT) and age matched CFTR−/− male mice were used to establish the myocardial I/R model. CFTR activator forskolin (FSK) was used to activate CFTR in mice. Hypoxia/reoxygenation (H/R) treatment was used for in vitro model in WT or CFTR−/− cardiomyocytes. The autophagy inhibitor 3-MA and activator rapamycin was used for inhibition or activation of autophagy, respectively. The mitochondrial membrane potential (MMP) and ATP concentration were detected. Immunofluorescence was performed for measurement of mitochondria. Oxidative factors reactive oxygen species (ROS), superoxide dismutase (SOD), malondiadehycle (MDA) and glutathione peroxidase (GSH-PX) were detected. The expression of CFTR, MMP-9, TNF-α, IL-8, LC3 II/I, beclin1, caspase-3, caspase-8, caspase-9, bax, bcl-2, p-62 and FUNDC1 was determined using western blotting or PCR. Results Knockdown of CFTR significantly increased the infraction volume and decreased the expression of autophagy related proteins beclin1 and LC3II/I in mice. In H/R cardiomyocytes, deficiency of CFTR by induced dysfunction of mitochondrial, decrease of ATP concentration and enhanced oxidative stress, as well as inhibited mitophagy and increased cell apoptosis related protein levels. When treated with 3-MA, the effects of overexpression of CFTR was remarkably reversed, while treatment of rapamycin significantly reversed the effects of inhibiting CFTR on both mitophagy, oxidative stress and cell apoptosis related proteins. The inhibition of FUNDC1 also reversed the above effects of overexpressing CFTR. Conclusion Inhibition of CFTR could promote myocardial I/R injury by suppressing FUNDC1-mediated mitophagy and activating of oxidative stress.

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Rhein protects against cerebral ischemic‑/reperfusion‑induced oxidative stress and apoptosis in rats

Cited by 37 publications

References 63 publications

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Rhein lysinate improves motor function in rats with spinal cord injury via inhibiting p38 MAPK pathway

Root of Angelica gigas Nakai ameliorates ischemic stroke-induced brain injury in mice through the activation of the PI3K/AKT/mTOR and MAPK pathways

CFTR improves myocardial ischemic/reperfusion injury through activating FUNDC1-mediated mitophagy and regulating ATP and mitochondrial functions

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