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1.
Acta cir. bras ; 38: e380123, 2023. graf, ilus
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1429535

Resumo

Purpose: Myocardial ischemia/reperfusion injury (MIRI) leads to myocardial tissue necrosis, which will increase the size of myocardial infarction. The study examined the protective effect and mechanism of the Guanxin Danshen formula (GXDSF) on MIRI in rats. Methods: MIRI model was performed in rats; rat H9C2 cardiomyocytes were hypoxia-reoxygenated to establish a cell injury model. Results: The GXDSF significantly reduced myocardial ischemia area, reduced myocardial structural injury, decreased the levels of interleukin (IL-1ß, IL-6) in serum, decreased the activity of myocardial enzymes, increased the activity of superoxide dismutase (SOD), and reduced glutathione in rats with MIRI. The GXDSF can reduce the expression of nucleotide- binding oligomerization domain, leucine-rich repeat and pyrin domain containing nod-like receptor family protein 3 (NLRP3), IL-1ß, caspase-1, and gasdermin D (GSDMD) in myocardial tissue cells. Salvianolic acid B and notoginsenoside R1 protected H9C2 cardiomyocytes from hypoxia and reoxygenation injury and reduced the levels of tumor necrosis factor α (TNF-α) and IL-6 in the cell supernatant, decreasing the NLRP3, IL-18, IL-1ß, caspase-1, and GSDMD expression in H9C2 cardiomyocytes. GXDSF can reduce the myocardial infarction area and alleviate the damage to myocardial structure in rats with MIRI, which may be related to the regulation of the NLRP3. Conclusion: GXDSF reduces MIRI in rat myocardial infarction injury, improves structural damage in myocardial ischemia injury, and reduces myocardial tissue inflammation and oxidative stress by lowering inflammatory factors and controlling focal cell death signaling pathways.


Assuntos
Animais , Ratos , Reperfusão Miocárdica , Traumatismo por Reperfusão , Ginsenosídeos/administração & dosagem , Proteína 3 que Contém Domínio de Pirina da Família NLR
2.
Acta cir. bras ; 38: e380823, 2023. graf, ilus
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1439113

Resumo

Purpose: To explore the protection of naringenin against oxygen-glucose deprivation/reperfusion (OGD/R)-induced HT22 cell injury, a cell model of cerebral ischemia/reperfusion (I/R) injury in vitro, focusing on SIRT1/FOXO1 signaling pathway. Methods: Cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, malondialdehyde (MDA) content, 4-hydroxynonenoic acid (4-HNE) level, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities were measured by commercial kits. Inflammatory cytokines levels were determined by enzyme-linked immunosorbent assay (ELISA). The protein expressions were monitored by Western blot analysis. Results: Naringenin significantly ameliorated OGD/Rinduced cytotoxicity and apoptosis in HT22 cells. Meanwhile, naringenin promoted SIRT1 and FOXO1 protein expressions in OGD/R-subjected HT22 cells. In addition, naringenin attenuated OGD/R-induced cytotoxicity, apoptosis, oxidative stress (the increased ROS, MDA and 4-HNE levels, and the decreased SOD, GSH-Px and CAT activities) and inflammatory response (the increased tumor necrosis factor-α, interleukin [IL]-1ß, and IL-6 levels and the decreased IL-10 level), which were blocked by the inhibition of the SIRT1/FOXO1 signaling pathway induced by SIRT1-siRNA transfection. Conclusion: Naringenin protected HT22 cells against OGD/R injury depending on its antioxidant and anti-inflammatory activities via promoting the SIRT1/FOXO1 signaling pathway.


Assuntos
Traumatismo por Reperfusão , Transdução de Sinais , Estresse Oxidativo , Mediadores da Inflamação , Flavanonas/administração & dosagem
3.
Acta cir. bras ; 38: e381123, 2023. tab, ilus
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1439107

Resumo

Purpose: Nontransmissible chronic diseases, such as diabetes mellitus (DM) and nephropathy, affect a significant portion of the population, often treated due to injuries that require healing and regeneration. To create an experimental model of associated comorbidities, for healing and regeneration studies, protocols for induction of nephropathy by ischemia and reperfusion (I/R) and induction of DM by injection of streptozotocin (STZ) were associated. Methods: Sixty-four mice (Mus musculus), female, adult, Swiss strain, weighing approximately 20 g, were divided into four groups: G1: control (n = 24), G2: nephropathy group (N) (n = 7), G3, DM (n = 9), and G4: N+DM (n = 24). Arteriovenous stenosis (I/R) of the left kidney was performed as the first protocol. The animals received a hyperlipidemic diet for 7 days after the injection of STZ (150 mg/kg, via i.p.) and an aqueous glucose solution (10%) for 24 h. The animals in the G3 and G4 groups were observed for 14 days before receiving the diet and STZ. The evolution of nephropathy was observed using a urine test strip and the DM, through the analysis of blood glucose with a reagent strip on a digital monitor. Results: The ischemic induction protocols of nephropathy and DM with STZ, associated, were sustainable, low-cost, and without deaths. There were alterations compatible with initial renal alterations, in the first 14 days, such as increased urinary density, pH alteration, presence of glucose, proteins and leukocytes, when compared to the control group. DM was confirmed by the presence of hyperglycemia 7 days after induction and its evolution after 14 days. The animals in the G4 group showed constant weight loss when compared to the other groups. It was possible to observe morphological alterations in the kidneys submitted to I/R, regarding coloration, during surgery and after the end of the observation period, in the volume and size of the left kidney, when compared to the contralateral kidney. Conclusion: It was possible to induce nephropathy and DM associated in the same animal, in a simple way, confirmed with rapid tests, without losses, providing a basis for future studies.


Assuntos
Animais , Feminino , Camundongos , Traumatismo por Reperfusão , Diabetes Mellitus Experimental , Nefropatias Diabéticas/fisiopatologia
4.
Acta cir. bras ; 38: e381323, 2023. graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1439117

Resumo

Purpose: Acute mesenteric ischemia (AMI) is a condition in pediatric surgery that ranges from intestine necrosis to death. Ischemic postconditioning (IPoC) methods were developed to reduce the damage caused by revascularization. This study aimed to evaluate the efficacy of these methods in an experimental weaning rat model. Methods: Thirty-two 21-day-old Wistar rats were allocated into four groups according to the surgical procedure performed: control, ischemia-reperfusion injury (IRI), local (LIPoC) and remote IPoC (RIPoC). At euthanasia, fragments of the intestine, liver, lungs, and kidneys were submitted to histological, histomorphometric, and molecular analyses. Results: In the duodenum, intestines, and kidneys histological alterations promoted by IRI were reversed by remote postconditioning method. In the distal ileum, the histomorphometric alterations could be reversed by the postconditioning methods with more evident effects promoted by the remote method. The molecular analysis found that the levels of expression of Bax (proapoptotic) and Bcl-XL (antiapoptotic) genes in the intestine were increased by IRI. These alterations were equally reversed by the postconditioning methods, with more evident effects of the remote method. Conclusions: IPoC methods positively reduced the damage caused by IRI in weaning rats.


Assuntos
Animais , Ratos , Traumatismo por Reperfusão , Ratos Wistar , Pós-Condicionamento Isquêmico/veterinária , Isquemia Mesentérica/veterinária , Antioxidantes
5.
Acta cir. bras ; 38: e381023, 2023. ilus, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1439116

Resumo

Purpose: To investigate the role of cyanidin-3-O-glucoside (C3G) in renal ischemia/reperfusion (I/R) injury and the potential mechanisms. Methods: Mouse models were established by clamping the left renal vessels, and in vitro cellular models were established by hypoxic reoxygenation. Results: Renal dysfunction and tissue structural damage were significantly higher in the I/R group. After treatment with different concentrations of C3G, the levels of renal dysfunction and tissue structural damage decreased at different levels. And its protective effect was most pronounced at 200 mg/kg. The use of C3G reduced apoptosis as well as the expression of endoplasmic reticulum stress (ERS)-related proteins. Hypoxia/reoxygenation (H/R)-induced apoptosis and ERS are dependent on oxidative stress in vitro. In addition, both AG490 and C3G inhibited the activation of JAK/STAT pathway and attenuated oxidative stress, ischemia-induced apoptosis and ERS. Conclusions: The results demonstrated that C3G blocked renal apoptosis and ERS protein expression by preventing reactive oxygen species (ROS) production after I/R via the JAK/STAT pathway, suggesting that C3G may be a potential therapeutic agent for renal I/R injury.


Assuntos
Animais , Camundongos , Traumatismo por Reperfusão , Sistema de Sinalização das MAP Quinases , Janus Quinases , Injúria Renal Aguda/fisiopatologia , Isquemia , Antocianinas/análise
6.
Acta cir. bras ; 38: e382523, 2023. graf, ilus
Artigo em Inglês | VETINDEX | ID: biblio-1447035

Resumo

Purpose: To investigate the role of puerarin on renal fibrosis and the underlying mechanism in renal ischemia and reperfusion (I/R) model. Methods: Rats were intraperitoneally injected with puerarin (50 or 100 mg/kg) per day for one week before renal I/R. The level of renal collagen deposition and interstitial fibrosis were observed by hematoxylin and eosin and Sirius Red staining, and the expression of α-smooth muscle actin (α-SMA) was examined by immunohistochemical staining. The ferroptosis related factors and TLR4/Nox4-pathway-associated proteins were detected by Western blotting. Results: Puerarin was observed to alleviate renal collagen deposition, interstitial fibrosis and the α-SMA expression induced by I/R. Superoxide dismutase (SOD) activities and glutathione (GSH) level were decreased in I/R and hypoxia/reoxygenation (H/R), whereas malondialdehyde (MDA) and Fe2+ level increased. However, puerarin reversed SOD, MDA, GSH and Fe2+ level changes induced by I/R and H/R. Besides, Western blot indicated that puerarin inhibited the expression of ferroptosis related factors in a dose-dependent manner, which further demonstrated that puerarin had the effect to attenuate ferroptosis. Moreover, the increased expression of TLR/Nox4-pathway-associated proteins were observed in I/R and H/R group, but puerarin alleviated the elevated TLR/Nox4 expression. Conclusions: Our results suggested that puerarin inhibited oxidative stress and ferroptosis induced by I/R and, thus, delayed the progression of renal fibrosis, providing a new target for the treatment of renal fibrosis.


Assuntos
Animais , Ratos , Fibrose , Traumatismo por Reperfusão , Estresse Oxidativo/efeitos dos fármacos , Insuficiência Renal Crônica , Ferroptose/efeitos dos fármacos
7.
Acta sci. vet. (Impr.) ; 51(supl.1): Pub. 865, 2023. ilus, tab, graf
Artigo em Português | VETINDEX | ID: biblio-1434678

Resumo

Background: Ischemic neuromyopathy is the most common reason for amputation in cats. In veterinary medicine, the use of prosthetic limbs is not widespread; therefore, in most cases total limb amputation is indicated. However, hyperbaric oxygen therapy (HBOT) is an alternative with several benefits for the treatment of vascular disorders with reperfusion, ischemia, and infection. Therefore, this study aimed to report the positive effects of HBOT on the treatment of ischemic neuromyopathy secondary to arterial thromboembolism on the patient's clinical improvement, and on the preparation of the patient for insertion of an osseointegrated prosthesis. Case: A 6-month-old mixed-breed kitten returned for treatment after undergoing surgery seven days earlier for reduction of traumatic diaphragmatic hernia, during which it suffered a cardiorespiratory arrest. The patient presented with acute pelvic limb paralysis with 24-h evolution, absent femoral pulse, plantar cushions and dorsal part of the limbs cold and pale. After supportive therapy and diagnosis of aortic thromboembolism by arterial Doppler, the patient started adjunctive treatment with HBOT from the first day of hospitalization. Sessions took place in an exclusive hyperbaric chamber for animals and lasted 60 min at a pressure of 2.5 absolute atmospheres and 100% oxygen, initially every 12 h. However, during the first 5 days of hospitalization, the distal region of both pelvic limbs began to show tissue devitalization and edema, and hematologic parameters showed changes on the 7th day. The right pelvic limb (RPL) showed more involvement of superficial tissues, extending to the tarsometatarsal joint region. After 8 days of hospitalization, the devitalized tissue was debrided. The RPL had an extensive devitalized area with exposed bone in the phalanges and necrosis in the pads. The left pelvic limb (LPL) suffered minor complications, with involvement of the phalangeal region. After 12 days, with HBOT every 48 h, exuberant granulation tissue was observed. After 17 days, the patient was discharged, and HBOT sessions were performed weekly. Gangrene of the midfoot and lack of proprioception were observed in RPL, while LPL showed bone divulsion of the 1st, 3rd, and 4th phalanges. Because of the poor prognosis for limb viability, the RPL was partially amputated, and a self-threaded intraosseous prosthesis was inserted. Discussion: The cardiorespiratory arrest that occurred during the surgical procedure to reduce the diaphragmatic hernia without thromboprophylaxis may have contributed to the peripheral ischemia. HBOT was proposed for the adjuvant treatment of ischemic injury because it is especially indicated for cases of ischemia-reperfusion injury. The main hematological parameters were evaluated at an average interval of 7 days. While the platelet count and hematocrit increased, the leukocytosis decreased. This demonstrates the benefit of oxygen therapy in the reported patient. The use of HBOT in orthopedic injuries is known to result mainly in stimulation of osteoblasts, promoting osseointegration of the prosthesis. We conclude that the adjuvant treatment with HBOT helped to preserve a large segment of both pelvic limbs, prevent the progression of necrosis, and provide a healthy bed for fixation of an osseointegrated prosthesis in the RPL, resulting in clinical improvement of the patient.


Assuntos
Animais , Feminino , Gatos , Tromboembolia/terapia , Tromboembolia/veterinária , Prótese Ancorada no Osso/veterinária , Oxigenoterapia Hiperbárica/veterinária
8.
Acta cir. bras ; 38: e381523, 2023. tab, ilus
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1439109

Resumo

Purpose: It was aimed to investigate the biochemical and immunohistochemical effects of ephedrine (EPH) in bilateral ovariectomized rats. Methods: Twenty-four Sprague Dawley female rats were divided into three groups: control group: The abdomen was opened and closed without any treatment; ischemia-reperfusion (IR) group: 2 h of ischemia followed by 2 h of reperfusion were allowed to cause IR injury; IR+EPH group: oral EPH solution (5 mg/kg) was administered for 28 days. Results: Biochemical parameters were statistically significant in group comparisons. Increased interleukin-6 (IL-6) expression, degenerative preantral and antral follicle cells and inflammatory cells around blood vessels were seen in IR group. Negative IL-6 expression was observed in seminal epithelial cells, preantral and antral follicle cells in IR+EPH group. While caspase-3 activity increased in granulosa cells and stromal cells in IR group, caspase-3 expression was negative in preantral and antral follicle cells in the germinal epithelium and cortex in IR+EPH group. Conclusion: The effect of apoptosis, which occurs with the signaling that starts in the cell nucleus, caused the cessation of the stimulating effect at the nuclear level after EPH administration, and a decrease in the antioxidative effect in IR damage and inflammation in the apoptotic process.


Assuntos
Animais , Feminino , Ratos , Ovário/citologia , Interleucina-6/fisiologia , Efedrina/análise , Caspase 3/fisiologia , Imuno-Histoquímica , Ratos Sprague-Dawley , Apoptose
9.
Acta cir. bras ; 38: e380423, 2023. tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1439115

Resumo

Purpose: Remote ischemic preconditioning (RIPC) confers cardioprotection against ischemia reperfusion (IR) injury. However, the precise mechanisms involved in RIPC-induced cardioprotection are not fully explored. The present study was aimed to identify the role of melatonin in RIPC-induced late cardioprotective effects in rats and to explore the role of H2 S, TNF-α and mitoKATP in melatoninmediated effects in RIPC. Methods: Wistar rats were subjected to RIPC in which hind limb was subjected to four alternate cycles of ischemia and reperfusion of 5 min duration by using a neonatal blood pressure cuff. After 24 h of RIPC or ramelteon-induced pharmacological preconditioning, hearts were isolated and subjected to IR injury on the Langendorff apparatus. Results: RIPC and ramelteon preconditioning protected the hearts from IR injury and it was assessed by a decrease in LDH-1, cTnT and increase in left ventricular developed pressure (LVDP). RIPC increased the melatonin levels (in plasma), H2 S (in heart) and decreased TNF-α levels. The effects of RIPC were abolished in the presence of melatonin receptor blocker (luzindole), ganglionic blocker (hexamethonium) and mitochondrial KATP blocker (5-hydroxydecanoic acid). Conclusion: RIPC produce delayed cardioprotection against IR injury through the activation of neuronal pathway, which may increase the plasma melatonin levels to activate the cardioprotective signaling pathway involving the opening of mitochondrial KATP channels, decrease in TNF-α production and increase in H2 S levels. Ramelteon-induced pharmacological preconditioning may also activate the cardioprotective signaling pathway involving the opening of mitochondrial KATP channels, decrease in TNF-α production and increase in H2 S levels.


Assuntos
Animais , Ratos , Troponina/fisiologia , Cardiotônicos , Precondicionamento Isquêmico , Melatonina/análise , Infarto do Miocárdio/veterinária , Ensaio de Imunoadsorção Enzimática/veterinária , Ratos Wistar/fisiologia , Mitocôndrias
10.
Acta cir. bras ; 37(10): e371004, 2022. graf, tab
Artigo em Inglês | VETINDEX | ID: biblio-1415430

Resumo

Purpose: The present study explored the role and mechanism involved in aprepitant-induced cardioprotective effects in rat model of ischemia-reperfusion injury. Methods: The isolated hearts of Wistar male albino rats were subjected to ischemia-reperfusion injury on Langendorff apparatus. The extent of myocardial injury was assessed by measuring lactate dehydrogenase 1 and CK-MB release in the coronary effluent. The rats were treated with aprepitant (5, 10 and 20 mg/kg) before isolating hearts. After injury, the levels of HIF-1α, p-AkT, p-GSK-3ß/GSK-3ß were measured in heart homogenates. LY294002 was employed as PI3K inhibitor. Results: Ischemia-reperfusion led to significant myocardial injury and decreased the levels of HIF-1α, p-AkT and ratio of p-GSK-3ß/GSK-3ß. Aprepitant attenuated myocardial injury and restored the biochemical changes in a dose-dependent manner. Pre-treatment with LY294002 (10 and 20 mg/kg) abolished aprepitant-mediated cardioprotective effects and restored the biochemical parameters in the heart homogenate. Conclusions: Aprepitant may be effective in preventing ischemia-reperfusion-induced myocardial injury, which may be due to activation of PI3K-AkT-GSK-3ß and HIF-1α signaling pathway.


Assuntos
Animais , Ratos , Cardiotônicos , Traumatismo por Reperfusão , Aprepitanto/administração & dosagem , Isquemia
11.
Acta cir. bras ; 37(9): e370904, 2022. ilus, tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1413622

Resumo

Purpose: This study investigated the effects of oral administration of Clostridium butyricum (C. butyricum) on inflammation, oxidative stress, and gut flora in rats with hepatic ischemia reperfusion injury (HIRI). Methods: The rats from C. butyricum group were given C. butyricum for 5 days. Then, hepatic ischemia for 30 min and reperfusion for 6 h were performed in all the rats. After the animals were sacrificed, alanine transaminase (ALT), aspartate aminotransferase (AST), lipopolysaccharide (LPS) in serum, short-chain fatty acids (SCFAs), and gut microbiota composition in feces, and malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), Toll-like receptor 4 (TLR4), nuclear factor-kappa Bp65 (NF-κBp65) and histological analysis in the liver were performed. Results: The rats given C. butyricum showed decreased ALT, AST, LPS, and MDA; improved GSH and histological damage; changes in SCFAs; declined TNF-α, IL-6, TLR4, and pNF-κBp65/NF-κBp65; and changes in the gut microbial composition, which decreased the Firmicutes/Bacteroidetes ratio and increased the relative abundance (RA) of probiotics. Conclusions: C. butyricum supplementation protected against HIRI by regulating gut microbial composition, which contributed to the decreased LPS and attenuation of inflammation and oxidative stress. These indicate C. butyricum may be a potent clinical preoperative dietary supplement for HIRI.


Assuntos
Animais , Ratos , Traumatismo por Reperfusão/veterinária , Substâncias Protetoras/administração & dosagem , Clostridium butyricum , Ácidos Graxos Voláteis , Estresse Oxidativo , Hepatopatias/terapia
12.
Acta cir. bras ; 37(1): e370102, 2022. ilus, tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1413333

Resumo

Introduction: Myocardial ischemia-reperfusion (I/R) injury is one of the mechanisms contributing to the high mortality rate of acute myocardial infarction. Purpose: This study intended to study the role of naringin in cardiac I/R injury. Methods: AC16 cells (human cardiomyocyte cell line) were subjected to oxygen-glucose deprivation/recovery (OGD/R) treatment and/or naringin pretreatment. Then, the apoptosis was examined by flow cytometry and Western blotting. The concentration of IL-6, IL-8 and TNF-α was measured by enzyme-linked immunosorbent assay (ELISA) kits. How naringin influenced microRNA expression was examined by microarrays and quantitative real-time polymerase chain reaction (qRT-PCR). Dual luciferase reporter assay was employed to evaluate the interaction between miR-126 and GSK-3ß. The GSK-3ß/ß-catenin signaling pathway was examined by Western blotting. Finally, rat myocardial I/R model was created to examine the effects of naringin in vivo. Results: Naringin pretreatment significantly decreased the cytokine release and apoptosis of cardiomyocytes exposed to OGD/R. Bioinformatical analysis revealed that naringin upregulated miR-126 expression considerably. Also, it was found that miR-126 can bind GSK-3ß and downregulate its expression, suggesting that naringin could decrease GSK-3ß activity. Next, we discovered that naringin increased ß-catenin activity in cardiomyocytes treated with OGD/R by inhibiting GSK-3ß expression. Our animal experiments showed that naringin pre-treatment or miR-126 agomir alleviated myocardial I/R. Conclusions: Naringin preconditioning can reduce myocardial I/R injury via regulating miR-126/GSK-3ß/ß-catenin signaling pathway, and this chemical can be used to treat acute myocardial infarction.


Assuntos
Animais , Ratos , Traumatismo por Reperfusão/tratamento farmacológico , Isquemia Miocárdica/tratamento farmacológico , Flavanonas/administração & dosagem , beta Catenina/análise
13.
Acta cir. bras ; 37(1): e370105, 2022. tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1364250

Resumo

Purpose: To evaluate how the induction of liver damage by ischemia and reperfusion affects the adipose tissue of lean and obese mice. Methods: Lean and diet-induced obese mice were subjected to liver ischemia (30 min) followed by 6 h of reperfusion. The vascular stromal fraction of visceral adipose tissue was analyzed by cytometry, and gene expression was evaluated by an Array assay and by RT-qPCR. Intestinal permeability was assessed by oral administration of fluorescein isothiocyanate (FITC)-dextran and endotoxemia by serum endotoxin measurements using a limulus amebocyte lysate assay. Results: It was found that, after liver ischemia and reperfusion, there is an infiltration of neutrophils, monocytes, and lymphocytes, as well as an increase in the gene expression that encode cytokines, chemokines and their receptors in the visceral adipose tissue of lean mice. This inflammatory response was associated with the presence of endotoxemia in lean mice. However, these changes were not observed in the visceral adipose tissue of obese mice. Conclusions: Liver ischemia and reperfusion induce an acute inflammatory response in adipose tissue of lean mice characterized by an intense chemokine induction and leukocyte infiltration; however, inflammatory alterations are already present at baseline in the obese adipose tissue and liver ischemia and reperfusion do not injure further.


Assuntos
Animais , Camundongos , Traumatismo por Reperfusão/veterinária , Interleucina-6 , Endotoxinas/análise , Gordura Intra-Abdominal/fisiopatologia , Inibidores do Fator de Necrose Tumoral/análise
14.
Acta cir. bras ; 37(7): e370701, 2022. graf, ilus
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1402968

Resumo

Purpose: Tanshinone IIA is a well-known lipophilic active constituent refined from traditional Chinese medicines, danshen. It has been previously demonstrated to possess various biological properties, including anti-inflammatory, antioxidant, promoting angiogenesis effect and so on. However, the mechanism of tanshinone IIA on myocardial ischemia-reperfusion injury (MI/RI) remains unclear. In this study, we investigated the effect of tanshinone IIA on MI/RI. Methods: MI/RI rat models were set up. Echocardiographic evaluation and hematoxylin and eosin staining were performed to analyze the cardiac function and morphology of MI/RI. Western blot was conducted for the detection of protein expression of pyrin domain containing 3 (NLRP3) and caspase-1 in heart tissues. Flow cytometry and real-time polymerase chain reaction were used for the detection of proinflammatory cytokines and Th17 cells differentiation. Results: We found that tanshinone IIA alleviated the myocardial damage of MI/RI, ameliorated the overall and local inflammatory reaction, and produced a cardioprotective effect by inhibiting of NLRP3 inflammasome activation and Th17/Treg cells differentiation. Conclusions: Our results highlighted the cardio-protective effect of tanshinone IIA on MI/RI and uncovered its underlying mechanism related to the NLRP3 inflammasome inhibition and the modulation of Th17/Treg cells differentiation.


Assuntos
Animais , Ratos , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Isquemia Miocárdica/tratamento farmacológico , Salvia miltiorrhiza/química , Células Th17 , Proteína 3 que Contém Domínio de Pirina da Família NLR , Medicina Tradicional Chinesa
15.
Acta cir. bras ; 37(1): e370101, 2022. ilus, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1413330

Resumo

Purpose: To investigate the role of peptidyl-prolyl cis/trans isomerase 1 (Pin1) on renal ischemia-reperfusion (I/R) injury and underlying mechanism. Methods: By establishing the in vitro and in vivo models of renal I/R, the role of Pin1 was explored by using molecular assays. Results: In renal I/R, endogenous Pin1 level was up-regulated in I/R-impaired kidney. Suppression of Pin1 with juglone afforded protection against I/R-mediated kidney dysfunction, and reduced I/R-induced endoplasmic reticulum (ER) stress in vivo. Consistent with the in vivo results, repression of Pin1 with juglone or gene knockdown with si-Pin1 conferred cytoprotection and restricted hypoxia/reoxygenation (H/R)-driven ER stress in HK-2 cells. Simultaneously, further study uncovered that Nrf-2/HO-1 signals was the association between Pin1 and ER stress in response to renal I/R. In addition, Nrf-2/HO-1 signal pathway was inactivated after kidney exposed to I/R, as indicated by the down-regulation of Nrf-2/HO-1 levels. Furthermore, inhibition of Pin1 remarkably rescued the inactivation ofNrf-2/HO-1. Conclusions: Pin1 modulated I/R-mediated kidney injury in ER stress manner dependent on Nrf2-HO-1 pathway in I/R injury.


Assuntos
Animais , Masculino , Ratos , Heme Oxigenase-1 , Fator 2 Relacionado a NF-E2/análise , Peptidilprolil Isomerase de Interação com NIMA/análise , Isquemia/veterinária , Reperfusão/veterinária , Ratos Sprague-Dawley , Estresse do Retículo Endoplasmático
16.
Acta cir. bras ; 37(4): e370407, 2022. graf, ilus
Artigo em Inglês | VETINDEX | ID: biblio-1383300

Resumo

Purpose: Myocardial ischemia/reperfusion (MI/R) injury refers to a pathological condition of treatment of myocardial infarction. Oxidative stress and inflammation are believed to be important mechanisms mediating MI/R injury. Kukoamine A (KuA), a sperm, is the main bioactive component extracted from the bark of goji berries. In this study, we wanted to investigate the possible effects of KuA on MI/R injury. Methods: In this experiment, all rats were divided into sham operation group, MI/R group, KuA 10 mg + MI/R group, KuA 20 mg + MI/R group. After 120 min of ischemia/reperfusion treatment, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal rates of rising and fall of left ventricular pressure (±dp/dtmax), and ischemic area were detected. Serum samples of rats in each group were collected. The enzyme activities of catalase (CAT), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), levels of malondialdehyde (MDA), CK muscle/brain (CK-MB), tumor necrosis factor (TNF), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) were detected using enzyme-linked immunosorbent assay (ELISA). The apoptosis of myocardium in each group was detected according to the instructions of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expressions of mammalian target of glycogen synthase kinase-3ß (GSH-3ß) and protein kinase B (Akt) mRNA level in myocardial tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR). Results: MI/R rats showed a significant increase in oxidative stress and inflammation. In addition, we showed that KuA significantly improved the myocardial function such as LVSP, left ventricular ejection fraction, +dp/dt, and -dp/dt. Here, it attenuated dose-dependent histological damage in ischemia-reperfused myocardium, which is associated with the enzyme activities of SOD, GSH-PX, and levels of MDA, IL-6, TNF-α, L-1ß. Conclusions: KuA inhibited gene expression of Akt/GSK-3ß, inflammation, oxidative stress and improved MR/I injury. Taken together, our results allowed us to better understand the pharmacological activity of KuA against MR/I injury.


Assuntos
Animais , Ratos , Reperfusão , Isquemia Miocárdica , Estresse Oxidativo , Inflamação , Infarto do Miocárdio
17.
Acta cir. bras. ; 36(1): e360104, 2021. graf, tab, ilus
Artigo em Inglês | VETINDEX | ID: vti-30538

Resumo

Purpose: To evaluate the protective effect of dexmedetomidine on gastric injury induced by ischemia reperfusion (I/R) in rats. Methods: A total of 18 male albino Wistar rats were divided groups as: gastric ischemia reperfusion (GIR), gastric ischemia reperfusion and 50 g/kg dexmedetomidine (DGIR) and sham operation (HG) group. After the third hour of reperfusion, the biochemical and histopathological examinations were performed on the removed stomach tissue. Results: Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were found to be significantly higher in GIR compared to HG (p 0.05). A statistically significant decrease was observed at the DGIR compared to the GIR for oxidants levels. Total glutathione (tGSH) and superoxide dismutase (SOD) levels were statistically significantly decreased at the GIR, and antioxidants levels were found to be significantly higher in the DGIR (p 0.05) There was no significant difference between HG and DGIR in terms of SOD (p = 0.097). The DGIRs epitheliums, glands and vascular structures were close to normal histological formation. Conclusions: Dexmedetomidine is found to prevent oxidative damage on the stomach by increasing the antioxidant effect. These results indicate that dexmedetomidine may be useful in the treatment of ischemia-reperfusion-related gastric damage.(AU)


Assuntos
Animais , Ratos , Dexmedetomidina/administração & dosagem , Isquemia/tratamento farmacológico , Isquemia/veterinária , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/veterinária , Antioxidantes
18.
Acta cir. bras ; 36(9): e360901, 2021. tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1345029

Resumo

ABSTRACT Purpose: To investigate the protective effect of parecoxib against lung ischemia-reperfusion injury (LIRI) in rats and the mechanism. Methods: Thirty rats were divided into sham-operated, LIRI and LIRI+parecoxib groups. LIRI model (ischemia for 60 min, followed by reperfusion for 120 min) was constructed in LIRI and LIRI+parecoxib groups. In LIRI+parecoxib group, 10 mg/kg parecoxib was given via femoral vein 15 min before ischemia beginning. At the end of the reperfusion, blood gas analysis, lung wet to dry mass ratio measurement, lung tissue biochemical determination and heme oxygenase-1 (HO-1) protein expression determination were performed. Results: Compared with LIRI group, in LIRI+parecoxib group the oxygenation index was significantly increased, the alveolar-arterial oxygen partial pressure difference was significantly decreased, the lung wet to dry mass ratio was significantly decreased, the lung tissue malondialdehyde content was significantly decreased, the lung tissue superoxide dismutase and myeloperoxidase activities were significantly increased, the lung tissue tumor necrosis factor α and interleukin 1β levels were significantly decreased, and the lung tissue HO-1 protein expression level was significantly increased (all P < 0.05). Conclusions: Parecoxib pretreatment can mitigate the LIRI in rats by reducing oxidative stress, inhibiting inflammatory response and up-regulating HO-1 expression in lung tissue.


Assuntos
Animais , Ratos , Traumatismo por Reperfusão/prevenção & controle , Traumatismo por Reperfusão/tratamento farmacológico , Lesão Pulmonar , Ratos Sprague-Dawley , Estresse Oxidativo , Heme Oxigenase-1 , Inflamação , Isoxazóis , Pulmão
19.
Acta cir. bras ; 36(3): e360305, 2021. tab, graf
Artigo em Inglês | LILACS, VETINDEX | ID: biblio-1284907

Resumo

ABSTRACT Purpose To evaluate the effect of creatine supplementation in the diet of rats subjected to ischemia and reperfusion of hind limbs. Methods Eighteen male Wistar rats were randomized to receive dietary creatine supplementation (G1) or no supplementation (G2), before being subjected to 4 h of ischemia followed by 4 h of reperfusion. In addition, 10 rats (G3) underwent the same surgical procedure, without ischemia, but with supplementation. After reperfusion, kidney and musculature were evaluated for histological damage and serum levels of alanine aminotransferase, urea and creatinine were obtained. Results The urea dosage showed significant differences between the groups (averages G1 = 155.1; G2 = 211.27; G3 = 160.42). Histological analysis found significant differences between G1 and G2 (but not between G1 and G3) in renal myoglobin cylinders and vacuolar degeneration variables and in hypereosinophilia and karyopyknosis variables in muscle fibers. There were no significant differences in the other variables studied. Conclusions Creatine supplementation was related to fewer histological lesions, as well as lower levels of plasma urea, which may suggest a protective effect against lesions caused by ischemia and reperfusion of posterior paws muscles in Wistar rats.


Assuntos
Animais , Masculino , Ratos , Traumatismo por Reperfusão/prevenção & controle , Creatina , Reperfusão , Ratos Wistar , Músculo Esquelético , Suplementos Nutricionais , Dieta , Isquemia , Rim
20.
Acta cir. bras. ; 36(3): e360305, 2021. tab
Artigo em Inglês | VETINDEX | ID: vti-30575

Resumo

Purpose: To evaluate the effect of creatine supplementation in the diet of rats subjected to ischemia and reperfusion of hind limbs. Methods: Eighteen male Wistar rats were randomized to receive dietary creatine supplementation (G1) or no supplementation (G2), before being subjected to 4 h of ischemia followed by 4 h of reperfusion. In addition, 10 rats (G3) underwent the same surgical procedure, without ischemia, but with supplementation. After reperfusion, kidney and musculature were evaluated for histological damage and serum levels of alanine aminotransferase, urea and creatinine were obtained. Results: The urea dosage showed significant differences between the groups (averages G1 = 155.1;G2 = 211.27; G3 = 160.42). Histological analysis found significant differences between G1 and G2 (but not between G1 and G3) in renal myoglobin cylinders and vacuolar degeneration variables and in hypereosinophilia and karyopyknosis variables in muscle fibers. There were no significant differences in the other variables studied. Conclusion: Creatine supplementation was related to fewer histological lesions, as well as lower levels of plasma urea, which may suggest a protective effect against lesions caused by ischemia and reperfusion of posterior paws muscles in Wistar rats.(AU)


Assuntos
Animais , Ratos , Suplementos Nutricionais , Creatina/administração & dosagem , Isquemia/veterinária , Traumatismo por Reperfusão/veterinária
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