Quercetin protects jejunal mucosa from experimental intestinal ischemia reperfusion injury by activation of CD68 positive cells

Čurgali, Kristína; Tóth, Štefan; Jonecová, Zuzana; Maretta, M.; Kalpakidis, Theodoros; Petriskova, Ivana; Kusnier, Matus; Šoltés, Ján; Švaňa, Martin; Čaprnda, Martin; Delev, Delian; Rodrigo, Luís; Mechírová, Eva; Kružliak, Peter

doi:10.1016/j.acthis.2017.11.001

Cited by 11 publications

(9 citation statements)

References 24 publications

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“…In another study about transport stress of pigs, quercetin-supplemented pigs showed lower levels of ROS and MDA in the intestine than the those in the control group ( Zou et al., 2016 ). As for the morphology changes, in an in vivo jejunal ischemia–reperfusion injury experiment in rats, the intestinal gland depth was significantly higher in the quercetin group, and deeper intestinal glands contributed to the faster recovery of the intestinal epithelium as it was the site of proliferation of epithelial cells ( Curgali et al., 2018 ). In our study, 200 ppm of quercetin significantly increased the crypt depth and decreased the ratio of villus height and crypt depth, which indicated faster recovery of the epithelium.…”

Section: Discussionmentioning

confidence: 99%

Effects of dietary quercetin on the antioxidative status and cecal microbiota in broiler chickens fed with oxidized oil

2020

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This study was conducted to evaluate the effects of quercetin on the antioxidant ability, intestinal barrier functions, and cecal microbiota in broiler chickens fed with oxidized soya oil. Four hundred eighty male Arbor Acres broilers were randomly assigned to 5 treatments, each involving 8 cages (12 birds per cage). The treatment groups were as follows: the control group, birds fed with basal diets containing oxidized oil, and birds fed with basal diets containing oxidized oil and supplemented with 200 ppm of quercetin, 400 ppm of quercetin, and 800 ppm of quercetin. The results showed that dietary supplementation with quercetin at a dose of 400 ppm or 800 ppm alleviated the increased serum malondialdehyde ( MDA ) level induced by oxidized oil on day 11 ( P = 0.005) and reversed the increased MDA level in the mucosa on day 11 ( P = 0.021). Quercetin significantly upregulated the transcription of nuclear factor erythroid 2–related factor 2 ( Nrf2 ) and its downstream genes such as catalase ( P < 0.001), superoxide dismutase 1 ( P < 0.001), glutathione peroxidase 2 ( P = 0.018), heme oxygenase-1 ( HO-1 ) ( P = 0.0), and thioredoxin ( P = 0.002) and reversed the mRNA expression of HO-1 ( P = 0.007) in the ileal mucosa. Tight junction protein 1 was only downregulated by oxidized oil ( P = 0.013). In addition, quercetin (800 ppm) alleviated the decreased mRNA expression of mucin 2 ( MUC2 ), which contributed to the intestinal chemical barrier ( P = 0.039). The supplemental dose of 400 ppm of quercetin was able to promote Lactobacillus in the cecum, which enhanced the gastrointestinal tract health. In summary, these results indicated that quercetin ameliorated the oxidized oil–induced oxidative stress by upregulating the transcription of Nrf2 and its downstream genes to restore redox balance and reinforced the intestinal barrier via higher expression and secretion of MUC2 and facilitating the growth of Lactobacillus in the cecum. Therefore, quercetin could be a potential feed additive that can be applied in poultry production for amelioration of oxidative stress caused by oxidized oil and preventing the potential invasion of exogenous pathogens.

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Section: Discussionmentioning

confidence: 99%

Effects of dietary quercetin on the antioxidative status and cecal microbiota in broiler chickens fed with oxidized oil

2020

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“…Commonly, mesenteric vascular occlusion in the rat, as a model used frequently to study ischemic injury to the intestine (i.e., [32][33][34][35][36][37]), acknowledges intestinal ischemic injury as a life-threatening condition that requires immediate attention and treatment of any potential underlying etiology, and then, distant organ damage (multiple organ dysfunction) [38], which, however, remains less discussed [32][33][34][35][36][37]. However, each of these studies favors specific management of the superior mesenteric artery injuries, with success depending on the agent's specific target.…”

Section: Introductionmentioning

confidence: 99%

“…However, each of these studies favors specific management of the superior mesenteric artery injuries, with success depending on the agent's specific target. These targets in the supposed main underlying disturbance (i.e., immune/inflammatory cellular reactions) [32][33][34][35][36][37] may be quite distinctive, i.e., 5-HT1B and 5-HT1D receptors (sumatriptan) [32], PARα receptors (fenofibrate) [33], toll-like receptors (TLRs) (N-acetylserotonin (NAS) [34], T cells (cyclosporine and rapamycin) [35], neutrophils (i.e., quercin) [36], and melatonin [37]. Contrarily, the prime cause, the occlusion of the superior mesenteric artery itself, has remained largely ignored [32][33][34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

“…These targets in the supposed main underlying disturbance (i.e., immune/inflammatory cellular reactions) [32][33][34][35][36][37] may be quite distinctive, i.e., 5-HT1B and 5-HT1D receptors (sumatriptan) [32], PARα receptors (fenofibrate) [33], toll-like receptors (TLRs) (N-acetylserotonin (NAS) [34], T cells (cyclosporine and rapamycin) [35], neutrophils (i.e., quercin) [36], and melatonin [37]. Contrarily, the prime cause, the occlusion of the superior mesenteric artery itself, has remained largely ignored [32][33][34][35][36][37]. Additionally, in these studies, the success of the beneficial effect on gastrointestinal lesion recovery was not confirmed with recovery of the distant organ damage, peripherally and centrally, which were not investigated [32][33][34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

“…Contrarily, the prime cause, the occlusion of the superior mesenteric artery itself, has remained largely ignored [32][33][34][35][36][37]. Additionally, in these studies, the success of the beneficial effect on gastrointestinal lesion recovery was not confirmed with recovery of the distant organ damage, peripherally and centrally, which were not investigated [32][33][34][35][36][37].…”

Section: Introductionmentioning

confidence: 99%

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Occlusion of the Superior Mesenteric Artery in Rats Reversed by Collateral Pathways Activation: Gastric Pentadecapeptide BPC 157 Therapy Counteracts Multiple Organ Dysfunction Syndrome; Intracranial, Portal, and Caval Hypertension; and Aortal Hypotension

et al. 2021

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Gastric pentadecapeptide BPC 157 therapy counteracts multiple organ dysfunction syndrome in rats, which have permanent occlusion of the superior mesenteric artery close to the abdominal aorta. Previously, when confronted with major vessel occlusion, its effect would rapidly activate collateral vessel pathways and resolve major venous occlusion syndromes (Pringle maneuver ischemia, reperfusion, Budd–Chiari syndrome) in rats. This would overwhelm superior mesenteric artery permanent occlusion, and result in local, peripheral, and central disturbances. Methods: Assessments, for 30 min (gross recording, angiography, ECG, pressure, microscopy, biochemistry, and oxidative stress), included the portal hypertension, caval hypertension, and aortal hypotension, and centrally, the superior sagittal sinus hypertension; systemic arterial and venous thrombosis; ECG disturbances; MDA-tissue increase; and multiple organ lesions and disturbances, including the heart, lung, liver, kidney, and gastrointestinal tract, in particular, as well as brain (cortex (cerebral, cerebellar), hypothalamus/thalamus, hippocampus). BPC 157 therapy (/kg, abdominal bath) (10 µg, 10 ng) was given for a 1-min ligation time. Results: BPC 157 rapidly recruits collateral vessels (inferior anterior pancreaticoduodenal artery and inferior mesenteric artery) that circumvent occlusion and ascertains blood flow distant from the occlusion in the superior mesenteric artery. Portal and caval hypertension, aortal hypotension, and, centrally, superior sagittal sinus hypertension were attenuated or eliminated, and ECG disturbances markedly mitigated. BPC 157 therapy almost annihilated venous and arterial thrombosis. Multiple organ lesions and disturbances (i.e., heart, lung, liver, and gastrointestinal tract, in particular, as well as brain) were largely attenuated. Conclusions: Rats with superior mesenteric artery occlusion may additionally undergo BPC 157 therapy as full counteraction of vascular occlusion-induced multiple organ dysfunction syndrome.

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Amplification of Cardioprotective Response of Remote Ischemic Preconditioning in Rats by Quercetin: Potential Role of Activation of mTOR-dependent Autophagy and Nrf2

Kandpal,

Kumar,

Singh

et al. 2024

Cardiovasc Drugs Ther

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Quercetin protects jejunal mucosa from experimental intestinal ischemia reperfusion injury by activation of CD68 positive cells

Cited by 11 publications

References 24 publications

Effects of dietary quercetin on the antioxidative status and cecal microbiota in broiler chickens fed with oxidized oil

Effects of dietary quercetin on the antioxidative status and cecal microbiota in broiler chickens fed with oxidized oil

Occlusion of the Superior Mesenteric Artery in Rats Reversed by Collateral Pathways Activation: Gastric Pentadecapeptide BPC 157 Therapy Counteracts Multiple Organ Dysfunction Syndrome; Intracranial, Portal, and Caval Hypertension; and Aortal Hypotension

Amplification of Cardioprotective Response of Remote Ischemic Preconditioning in Rats by Quercetin: Potential Role of Activation of mTOR-dependent Autophagy and Nrf2

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