Modulatory effects of resveratrol on endoplasmic reticulum stress-associated apoptosis and oxido-inflammatory markers in a rat model of rotenone-induced Parkinson's disease

Gaballah, Hanaa Hibishy; Zakaria, Soha S.; ElBatsh, Maha M.; Tahoon, Nahid

doi:10.1016/j.cbi.2016.03.023

Cited by 110 publications

(97 citation statements)

References 48 publications

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“…43 Moreover, resveratrol has been reported to modulate ER stress-associated apoptosis and inflammatory markers in a rat model of Parkinson's disease. 44 Consistent with the expression of NF-κB in the present study, our data revealed that activation of ER stress, evidenced by the increased expression of p-PERK, p-IRE1 and ATF6, is involved in the development of VPN induced by IR. It should be noted that administration of resveratrol immediately before reperfusion significantly F I G U R E 5 Effects of resveratrol on endoplasmic reticulum stress sensors in the rat sciatic nerves after vasculitic peripheral neuropathy induced by ischaemia-reperfusion (IR) in the femoral artery (n = 6 in each group).…”

Section: Discussionsupporting

confidence: 91%

“…Resveratrol has been reported to reduce tunicamycin‐induced cell damage and apoptosis in neuronal HT22 cells through inhibiting the expression of ER stress‐related proteins . Moreover, resveratrol has been reported to modulate ER stress‐associated apoptosis and inflammatory markers in a rat model of Parkinson's disease . Consistent with the expression of NF‐κB in the present study, our data revealed that activation of ER stress, evidenced by the increased expression of p‐PERK, p‐IRE1 and ATF6, is involved in the development of VPN induced by IR.…”

Section: Discussionsupporting

confidence: 88%

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Resveratrol alleviates nuclear factor‐κB‐mediated neuroinflammation in vasculitic peripheral neuropathy induced by ischaemia–reperfusion via suppressing endoplasmic reticulum stress

Pan

Lin

Chuang

et al. 2019

Clin Exp Pharma Physio

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Vasculitic peripheral neuropathy (VPN) arises from an inflammatory obstruction in the blood vessels supplying peripheral nerves and subsequent ischaemic insults, which exhibits the clinical features of neuropathic pain and impaired peripheral nerve function. VPN induced by ischaemia–reperfusion (IR) has been reported to involve nuclear factor‐κB (NF‐κB)‐mediated neuroinflammation. Recent studies have suggested that endoplasmic reticulum (ER) stress has been implicated in the development of peripheral neuropathies. Resveratrol possesses a potent anti‐inflammatory capacity. We hypothesized that resveratrol may exert a protective effect against VPN through modulating the interrelated ER stress and NF‐κB pathways. Male Sprague‐Dawley rats were allocated into five groups: sham, sham + resveratrol 40 mg/kg (R40), IR, IR + R20 and IR + R40. VPN was induced by occluding the right femoral artery for 4 hours followed by reperfusion. Our data have shown that VPN induced by IR led to hind paw mechanical allodynia, heat hyperalgaesia, and impaired motor nerve conduction velocity (MNCV). With resveratrol intervention, the behavioural parameters were improved in a dose‐dependent manner and the MNCV levels were increased as well. The molecular data revealed that VPN induced by IR significantly increased the expression of NF‐κB as well as the ER stress sensor proteins, protein kinase RNA‐like endoplasmic reticulum kinase, inositol‐requiring enzyme 1 and activating transcription factor 6 in the sciatic nerves. More importantly, resveratrol significantly attenuated the expression of NF‐κB and the ER stress sensor proteins after IR. In conclusion, resveratrol alleviates VPN induced by IR. The mechanisms may involve modulating NF‐κB‐mediated neuroinflammation via suppressing ER stress.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 88%

Resveratrol alleviates nuclear factor‐κB‐mediated neuroinflammation in vasculitic peripheral neuropathy induced by ischaemia–reperfusion via suppressing endoplasmic reticulum stress

Pan

Lin

Chuang

et al. 2019

Clin Exp Pharma Physio

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“…RES pretreatment also has neuroprotective effects against cerebral ischemia/reperfusion injury by activation of Nrf2 and upregulation of HO-1 in vivo (133, 134). In addition, Gaballah and colleagues recently observed that RES increased Nrf2 DNA binding activity in the rotenone model of neuronal oxidative stress in experimental PD (135). …”

Section: Phytochemicals With Nrf2-are Activating Abilitymentioning

confidence: 99%

Preventive and Protective Roles of Dietary Nrf2 Activators Against Central Nervous System Diseases

Sun

Yang

Leak

et al. 2017

CNSNDDT

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Central nervous system diseases are major health issues and are often associated with disability or death. Most central nervous system disorders are characterized by high levels of oxidative stress. Nuclear factor erythroid 2 related factor (Nrf2) is known for its ability to regulate the expression of a series of enzymes with antioxidative, prosurvival, and detoxification effects. Under basal conditions, Nrf2 forms a complex with Kelch-like ECH associated protein 1, leading to Nrf2 inactivation via ubiquitination and degradation. However, following exposure of Keap1 to oxidative stress, Nrf2 is released from Keap1, activated, and translocated into the nucleus. Upon nuclear entry, Nrf2 binds to antioxidant response elements (ARE), thereby inducing the expression of genes such as glutathione s-transferase, heme oxygenase 1, and NADPH quinine oxidoreductase 1. Many dietary phytochemicals have been reported to activate the protective Nrf2/ARE pathway. Here, we review the preventive and protective effects of dietary Nrf2 activators against CNS diseases, including stroke, traumatic brain injury, Alzheimer’s disease, and Parkinson’s disease.

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“…Recently, we have shown that RES prevented tau hyperphosphorylation and memory deficits in cadmium chloride (CdCl 2 )‐induced rat's model of neurodegeneration by increasing GSH levels, inhibition of ROS, downregulation of Bax, and upregulation of Bcl‐2, mediated by activation of AMPK/PI3K/Akt axis activity . Also, RES prevented neural apoptosis and preserved motor and memory function in rotenone‐induced Parkinson's disease and postoperative cognitive dysfunction animal models by inhibition of ER stress and UPR‐related proteins . However, a consensus is currently showing that most of health benefits of RES are due to its ability to enhance SIRT1 levels and activity …”

Section: Introductionmentioning

confidence: 99%

Resveratrol protects against cadmium chloride‐induced hippocampal neurotoxicity by inhibiting ER stress and GAAD 153 and activating sirtuin 1/AMPK/Akt

Shati

2019

Environmental Toxicology

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This study investigated whether the apoptotic effect induced by cadmium chloride (CdCl2) in rat's hippocampi and neuroprotection afforded by resveratrol (RES) are mediated by modulation of ER stress and involve sirtuin 1 (SIRT1)/AMPK/Akt axis. Adult male Wistar rats were divided into four groups (n = 24/group) as control, control + RES (300 mg/kg), CdCl2 (5 mg/kg), and CdCl2 + RES. All treatments were conducted orally for 45 days. Also, cultured hippocampal cells were treated with CdCl2 in the presence or absence of RES and with or without preincubation with SIRT1, AMPK, or PI3K inhibitors. CdCl2 impaired retention and spatial memories of rats and reduced levels and activities of SIRT1 and inhibited AMPK/Akt axis in their hippocamapi where SIRT1 was the upstream regulator. It also enahnced hippocampal levels of reactive oxygen species (ROS) and expression of caspase‐12 and caspase‐3, depleted glutathione (GSH) levels, and activated GRP78, activating transcription factor‐6, GAAD 153, X‐box binding protein‐1 arms of ER stress. On the contrary, RES coadminsitration completley abolished all these events. Interstingly and in control rats, RES not only increased levels of GSH, but also enhenced protein levels of B‐cell lymphoma 2 (Bcl‐2) and dwonregulated GAAD 153. In both control and CdCl2‐treated rats, pharmacological inhibtion of SIRT1, AMPK, and Akt compleltely abolished all effects afforded by RES. In conclusion, CdCl2‐induced hippocampal apopotis is associated with reduction of SIRT1/AMPK/Akt activity levels, ROS generation, downregulation of Bcl‐2, and activities, activation of ER stress, and GAAD 153, whereas RES is able to reverse these effects through activation of SIRT1/AMPK/Akt.

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Modulatory effects of resveratrol on endoplasmic reticulum stress-associated apoptosis and oxido-inflammatory markers in a rat model of rotenone-induced Parkinson's disease

Cited by 110 publications

References 48 publications

Resveratrol alleviates nuclear factor‐κB‐mediated neuroinflammation in vasculitic peripheral neuropathy induced by ischaemia–reperfusion via suppressing endoplasmic reticulum stress

Resveratrol alleviates nuclear factor‐κB‐mediated neuroinflammation in vasculitic peripheral neuropathy induced by ischaemia–reperfusion via suppressing endoplasmic reticulum stress

Preventive and Protective Roles of Dietary Nrf2 Activators Against Central Nervous System Diseases

Resveratrol protects against cadmium chloride‐induced hippocampal neurotoxicity by inhibiting ER stress and GAAD 153 and activating sirtuin 1/AMPK/Akt

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