Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?

Topaloğlu, Naci; Memi, Gülsün; Kaner, Tuncay; Deniz, Mustafa; Şahin, Önder; Güven, Mustafa; Çoşar, Murat

doi:10.3906/sag-1402-64

Cited by 5 publications

(4 citation statements)

References 33 publications

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“…Arda-Pirincci et al found that subcutaneous treatment with a GLP-2 analogue reversed morphological damage, oxidative stress, and cell apoptosis by markedly reducing lipid peroxidation in experimental mice with lung injuries [ 21 ]. Similar results were observed in another study, which revealed GLP-2 treatment could decrease oxidative damage in a rat model of cerebral ischemia/reperfusion [ 22 ]. However, so far, there have been no studies to date on the effect of GLP-2 on antioxidant activity in a TPN model, and the mechanisms of this property have yet to be elucidated.…”

Section: Introductionsupporting

confidence: 90%

GLP-2 Prevents Intestinal Mucosal Atrophy and Improves Tissue Antioxidant Capacity in a Mouse Model of Total Parenteral Nutrition

Lei

Wang

et al. 2016

Nutrients

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We investigated the effects of exogenous glucagon-like peptide-2 (GLP-2) on mucosal atrophy and intestinal antioxidant capacity in a mouse model of total parenteral nutrition (TPN). Male mice (6–8 weeks old) were divided into three groups (n = 8 for each group): a control group fed a standard laboratory chow diet, and experimental TPN (received standard TPN solution) and TPN + GLP-2 groups (received TPN supplemented with 60 µg/day of GLP-2 for 5 days). Mice in the TPN group had lower body weight and reduced intestinal length, villus height, and crypt depth compared to the control group (all p < 0.05). GLP-2 supplementation increased all parameters compared to TPN only (all p < 0.05). Intestinal total superoxide dismutase activity and reduced-glutathione level in the TPN + GLP-2 group were also higher relative to the TPN group (all p < 0.05). GLP-2 administration significantly upregulated proliferating cell nuclear antigen expression and increased glucose-regulated protein (GRP78) abundance. Compared with the control and TPN + GLP-2 groups, intestinal cleaved caspase-3 was increased in the TPN group (all p < 0.05). This study shows GLP-2 reduces TPN-associated intestinal atrophy and improves tissue antioxidant capacity. This effect may be dependent on enhanced epithelial cell proliferation, reduced apoptosis, and upregulated GRP78 expression.

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Section: Introductionsupporting

confidence: 90%

GLP-2 Prevents Intestinal Mucosal Atrophy and Improves Tissue Antioxidant Capacity in a Mouse Model of Total Parenteral Nutrition

Lei

Wang

et al. 2016

Nutrients

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“…MPO is a lysosomal enzyme released from leukocytes in response to oxidative stress. [ 17 ] IL-6 is a cytokine that has an important role in hematopoiesis, host defense, inflammation, and tissue regeneration. In many studies, the increase in MPO and IL-6 after testicular I/R was associated with and elucidated by inflammation.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of osthole on testicular ischemia/reperfusion injury in rats

Kocaman

Günendi

Dörterler

et al. 2022

Ulus Travma Acil Cerrahi Derg

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BACKGROUND: Testicular torsion is a urological emergency that requires urgent surgical intervention which results in testicular loss if not diagnosed and treated in a timely fashion. Ischemic tissue damage with oxygen deficiency, which starts with the decrease in blood flow to the tissue, continues to increase with the reoxygenation of the damaged tissues as soon as reperfusion is achieved. In various studies, osthole has also been shown to reduce cerebral, spinal cord, intestinal, renal, and myocardial ischemia/perfusion (I/R) damage. The aim of this study is to examine the effects of osthole on testicular I/R injury. METHODS: 28 Wistar-albino rats were randomly divided into four experimental groups (n=7). Group 1 was the sham operation group. In Group 2 (I/R), 3-h ischemia was created by rotating the testis 720° clockwise, followed by 3 h of reperfusion. In Group 3 (I/R + single dose of Osthole), 20 mg/kg ostol was administered intraperitoneally half an hour before detorsion after 3 h of torsion. The testis was detorsioned. Three h of detorsion was applied. In Group 4 (I/R + twice doses of Osthole), 20 mg/kg ostol was administered intraperitoneally half an hour before detorsion, followed by 3-h torsion. The testis was released and detorsioned. Half an hour after the detorsion, an intraperitoneal dose of 20 mg/kg osthole was administered again. Detorsion was done for 3 h. All rats were sacrificed after 6 h and right orchiectomy was performed for blood for biochemical analysis and histopathological sample. RESULTS: Glutathion, nuclear respiratory factor 2, Superoxide dismutase, and 8-hydroxydeoxyguanosine levels were decreased in I/R rats, while interleukin-6, malondialdehyde, and myeloperoxidase levels were increased. While caspase 3, caspase 8, caspase 9, and TUNEL showed moderate immunopositive tissues immunohistochemically in rats with I/R damage, mild immunopositive tissues were detected in Group 3 and Group 4. In the histochemical examination, degenerative tubule structure and separation of epithelial cells were observed in I/R rats, while partially healed testicular tissue was detected in Group 3 and Group 4. CONCLUSION: In our study, we observed that osthole reduced oxidative damage, suppressed the inflammatory process, prevented apoptosis, and reduced cell damage. We think that with repeated doses, cellular damage would gradually decline.

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“…Importantly, GLP-2 signaling had clear neuroprotective effects in a re-perfusion stroke model in rats [9] and improved learning, memory and cognitive ability in a cerebral ischemia mouse model of vascular dementia [8]. GLP-2 decreased oxidative damage in the cerebral ischemia/reperfusion model, in which GLP-2 increased the MDA (malondialdehyde) levels and MPO (myeloperoxidase) activity, and reduced the number of apoptotic hippocampal neurons [7]. In addition, the protective effect of GLP-2 on memory impairment in lipopolysaccharide (LPS)treated mice were investigated, and it was found that GLP-2 can reduce the inflammation response and protect and improve memory function [12].…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that GLP-2 has protective effects in a mouse model of sporadic Alzheimer's disease (AD) in which streptozotocin is injected directly into the brain to induce neurodegenerative processes and insulin desensitization [5], and that the drug reduces obesity-related neuroinflammation [6]. It furthermore is neuroprotective in a cerebral ischemia/reperfusion model of stroke [7], in an animal model of vascular dementia [8], chronic cerebral hypoperfusion [9] and in several mouse models of depression [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

A GLP-2 Analogue Protects SH-SY5Y and Neuro-2a Cells Against Mitochondrial Damage, Autophagy Impairments and Apoptosis in a Parkinson Model

Su¹,

Zhang

et al. 2020

Drug Res (Stuttg)

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Glucagon-like peptide-2 (GLP-2) is a peptide hormone that belongs to the glucagon-derived peptide family. We have previously shown that analogues of the sister hormone Glucagon-like peptide-1 (GLP-1) showed neuroprotective effects. Here we investigated the effect of a GLP-2 agonist in a cell model of Parkinsonʼs disease (PD) created by treating SH-SY5Y or Neuro-2a cells with 1-Methyl-4-phenyl-pyridine ion (MPP+). Cell viability and cell cytotoxicity was detected by MTT and LDH assays, respectively. The protein expression levels of mitochondrial, autophagy and apoptotic biomarkers including PGC-1α, Mfn2, IRE1, ATG7, LC3B, Beclin1 and Bcl-2 were detected by western blot. Mitochondrial superoxide was detected by MitoSOX Red. In addition, mitochondrial morphology, autophagosome and apoptotic corpuscles were observed by transmission electron microscope (TEM). We found that the GLP-1 and the GLP-2 agonists both protect cells against mitochondrial damage, autophagy impairments and apoptosis induced by MPP+both in SH-SY5Y and Neuro-2a cells. Cell signaling for mitogenesis was enhanced, and oxidative stress levels much reduced by the drugs. This demonstrates for the first time the neuroprotective effects of a GLP-2 analogue in PD cellular models, in which oxidative stress, autophagy and apoptosis play crucial roles. The protective effects were comparable to those seen with the GLP-1 analogue liraglutide. The results suggest that not only GLP-1, but also GLP-2 has neuroprotective properties and may be useful as a novel treatment of PD.

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Does Glp-2 have a protective effect on cerebral ischemia/reperfusion model?

Cited by 5 publications

References 33 publications

GLP-2 Prevents Intestinal Mucosal Atrophy and Improves Tissue Antioxidant Capacity in a Mouse Model of Total Parenteral Nutrition

GLP-2 Prevents Intestinal Mucosal Atrophy and Improves Tissue Antioxidant Capacity in a Mouse Model of Total Parenteral Nutrition

Protective effect of osthole on testicular ischemia/reperfusion injury in rats

A GLP-2 Analogue Protects SH-SY5Y and Neuro-2a Cells Against Mitochondrial Damage, Autophagy Impairments and Apoptosis in a Parkinson Model

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