Weight loss: indication of brain damage and effect of combined normobaric oxygen and ethanol therapy after stroke

Cai, Lining; Xu, Geng; Hussain, Mohammed; Liu, Zongjian; Gao, Zhi; Liu, Shimeng; Du, Hongguang; Ji, Xunming; Ding, Yuchuan

doi:10.1179/1743132815y.0000000033

Cited by 6 publications

(3 citation statements)

References 25 publications

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“…Protein levels of PKC-δ, p-Akt, Caspase-3, Bax, and Bcl-XL were detected by western blotting. Brain tissues containing the frontoparietal cortex and dorsolateral striatum were processed as described previously [34] and incubated with primary antibodies (polyclonal rabbit anti-PKC-δ at 1:5000, Santa Cruz Biotechnology, Santa Cruz, CA, USA; polyclonal rabbit anti-phospho-Akt 1:1000, Cell Signaling Technology, Danvers, MA, USA; rabbit polyclonal anti-caspase-3 antibody, 1:1000, Santa Cruz Biotechnology, Santa Cruz, CA, USA; rabbit polyclonal anti-cleaved caspase-3 antibody, 1:5000, Santa Cruz Biotechnology, Santa Cruz, CA, USA; rabbit polyclonal anti-BAX antibody, 1:500, Santa Cruz Biotechnology, Santa Cruz, CA, USA; mouse monoclonal anti-Bcl-XL, 1:200, Santa Cruz Biotechnology, Santa Cruz, CA, USA) at 4 • C. Western blot images were analyzed by an image analysis program (ImageJ 1.42, National Institutes of Health, Bethesda, MD, USA) to quantify protein expression in terms of relative image density.…”

Section: Western Blottingmentioning

confidence: 99%

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway

et al. 2019

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Phenothiazine treatment has been shown to reduce post-stroke ischemic injury, though the underlying mechanism remains unclear. This study sought to confirm the neuroprotective effects of phenothiazines and to explore the role of the NOX (nicotinamide adenine dinucleotide phosphate oxidase)/Akt/PKC (protein kinase C) pathway in cerebral apoptosis. Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO) for 2 h and were randomly divided into 3 different cohorts: (1) saline, (2) 8 mg/kg chlorpromazine and promethazine (C+P), and (3) 8 mg/kg C+P as well as apocynin (NOX inhibitor). Brain infarct volumes were examined, and cell death/NOX activity was determined by assays. Western blotting was used to assess protein expression of kinase C-δ (PKC-δ), phosphorylated Akt (p-Akt), Bax, Bcl-XL, and uncleaved/cleaved caspase-3. Both C+P and C+P/NOX inhibitor administration yielded a significant reduction in infarct volumes and cell death, while the C+P/NOX inhibitor did not confer further reduction. In both treatment groups, anti-apoptotic Bcl-XL protein expression generally increased, while pro-apoptotic Bax and caspase-3 proteins generally decreased. PKC protein expression was decreased in both treatment groups, demonstrating a further decrease by C+P/NOX inhibitor at 6 and 24 h of reperfusion. The present study confirms C+P-mediated neuroprotection and suggests that the NOX/Akt/PKC pathway is a potential target for efficacious therapy following ischemic stroke.

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Section: Western Blottingmentioning

confidence: 99%

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway

et al. 2019

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“…The reason for this dramatic and prolonged weight loss after stroke is unclear and could involve several mechanisms, including reduced food intake and/or raised energy expenditure, possibly via the action of inflammatory mediators. Acute weight loss after experimental stroke can correlate positively with ischaemic damage [30,58], although this correlation is not always observed [18]. Here, the degree of weight loss over 49 days did not directly correlate with initial damage at 48 h, suggesting that post-stroke weight loss may be caused by factors secondary to the initial injury, and develop during recovery.…”

Section: Discussionmentioning

confidence: 77%

Stroke Induces Prolonged Changes in Lipid Metabolism, the Liver and Body Composition in Mice

Haley

White

Roberts

et al. 2019

Transl. Stroke Res.

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During recovery, stroke patients are at risk of developing long-term complications that impact quality of life, including changes in body weight and composition, depression and anxiety, as well as an increased risk of subsequent vascular events. The aetiologies and time-course of these post-stroke complications have not been extensively studied and are poorly understood. Therefore, we assessed long-term changes in body composition, metabolic markers and behaviour after middle cerebral artery occlusion in mice. These outcomes were also studied in the context of obesity, a common stroke co-morbidity proposed to protect against post-stroke weight loss in patients. We found that stroke induced long-term changes in body composition, characterised by a sustained loss of fat mass with a recovery of lean weight loss. These global changes in response to stroke were accompanied by an altered lipid profile (increased plasma free fatty acids and triglycerides) and increased adipokine release at 60 days. After stroke, the liver also showed histological changes indicative of liver damage and a decrease in plasma alanine aminotransferase (ALT) was observed. Stroke induced depression and anxiety-like behaviours in mice, illustrated by deficits in exploration, nest building and burrowing behaviours. When initial infarct volumes were matched between mice with and without comorbid obesity, these outcomes were not drastically altered. Overall, we found that stroke induced long-term changes in depressive/anxiety-like behaviours, and changes in plasma lipids, adipokines and the liver that may impact negatively on future vascular health.

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“…Weight loss has occurred after CIRI in both NG and T1DM rats so that T1DM rats are lighter than NG rats at both baseline and 24 h after 75‐min ischemia. Studies have shown a positive correlation between infarct volume and weight loss after acute stroke (Cai et al., 2015 ). A greater weight loss in T1DM rats is probably related to the increased severity of CIRI when compared to NG rats.…”

Section: Discussionmentioning

confidence: 99%

Melatonin mitigates type 1 diabetes‐aggravated cerebral ischemia‐reperfusion injury through anti‐inflammatory and anti‐apoptotic effects

Cheung

2023

Brain and Behavior

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IntroductionCerebral ischemia and diabetes mellitus (DM) are common diseases that often coexist and interact with each other. DM doubles the risk of ischemic stroke, and cerebral ischemia causes stress‐induced hyperglycemia. Most experimental stroke studies used healthy animals. Melatonin is neuroprotective against cerebral ischemia–reperfusion injury (CIRI) in non‐DM, normoglycemic animals through anti‐oxidant effect, anti‐inflammation, and anti‐apoptosis. Previous studies have also reported a negative correlation between hyperglycemia and urinary melatonin metabolite.ObjectivesThe present study investigated the effects of type 1 DM (T1DM) on CIRI in rats and the role of melatonin against CIRI in T1DM animals.ResultsOur results revealed that T1DM aggravated CIRI, leading to greater weight loss, increased infarct volume, and worse neurological deficit. T1DM aggravated the post‐CIRI activation of nuclear factor kappa B (NF‐κB) pathway and increase in pro‐apoptotic markers. A single intraperitoneal injection of melatonin at 10 mg/kg given 30 min before ischemia onset attenuated CIRI in T1DM rats, resulting in less weight loss, decreased infarct volume, and milder neurological deficit when compared with the vehicle group. Melatonin treatment achieved anti‐inflammatory and anti‐apoptotic effects with reduced NF‐κB pathway activation, reduced mitochondrial cytochrome C release, decreased calpain‐mediated spectrin breakdown product (SBDP), and decreased caspase‐3‐mediated SBDP. The treatment also led to fewer iNOS+ cells, milder CD‐68+ macrophage/microglia infiltration, decreased TUNEL+ apoptotic cells, and better neuronal survival.ConclusionsT1DM aggravates CIRI. Melatonin treatment is neuroprotective against CIRI in T1DM rats via anti‐inflammatory and anti‐apoptotic effects.

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Weight loss: indication of brain damage and effect of combined normobaric oxygen and ethanol therapy after stroke

Abstract: Degree of weight loss after stroke is largely associated with severity of infarction as well as damage reduction after treatment administration.

Cited by 6 publications

References 25 publications

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway

Stroke Induces Prolonged Changes in Lipid Metabolism, the Liver and Body Composition in Mice

Melatonin mitigates type 1 diabetes‐aggravated cerebral ischemia‐reperfusion injury through anti‐inflammatory and anti‐apoptotic effects

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