scholarly journals Effect of hydration with Ringer's solution submitted to magnetic field in an experimental model of hepatic ischemia-reperfusion injury in rats

2018 ◽  
Vol 9 (2) ◽  
pp. 44-53
Author(s):  
Juliana Mendonça Freire ◽  
Jeovana Pinheiro Fernandes de Souza ◽  
Italo Medeiros Azevedo ◽  
Fabio Medeiros de Azevedo ◽  
Artur Da Silva Carriço ◽  
...  

Purpose: To evaluate the effect of hydration with Ringer's solution submitted to magnetic field in experimental model of hepatic ischemia/reperfusion in rats. Methods: Wistar rats weighing 389.58±46.88g were randomly allocated into 2 groups: control group (n = 6) - Hepatic ischemia/reperfusion and hydration with Ringer's solution; and test group (n = 6) - Hepatic ischemia/reperfusion and hydration with Ringer submitted to magnetic field of 20 mT during 2 hours. After anesthesia with ketamine 70 mg/kg and xylazine 7 mg/kg i.p., the animals were weighed and operated by aseptic technique. The ischemia of the median and left liver lobes was induced for 30 minutes using a vascular clip. Then, i.v. hydration with 3 ml of Ringer in the control group, and 3 ml of magnetized Ringer’s solution in the test group. After 24 hours, blood sample and fragment of the left liver lobe were collected for the determination of AST, ALT, ALP and albumin levels, and histopathological examination. Results: There was no significant difference in comparison of the rats weight loss, biochemical measurements and histopathological scores between the groups (p>0.05). Conclusion: The hydration with Ringer's solution submitted to magnetic field after hepatic ischemia/reperfusion in rats did not alter liver function tests neither histopathological scores, comparing with the control group.

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 8-13 ◽  
Author(s):  
Raimundo José Cunha Araújo Júnior ◽  
Raimundo Gerônimo da Silva Júnior ◽  
Marcelo Pinho Pessoa de Vasconcelos ◽  
Sérgio Botelho Guimarães ◽  
Paulo Roberto Leitão de Vasconcelos ◽  
...  

PURPOSE: To evaluate the effects of pre-conditioning with L-alanyl- glutamine (L-Ala-Gln) in rats subjected to total hepatic ischemia. METHODS: Thirty Wistar rats, average weight 300g, were randomly assigned to 3 groups (n=10): G-1 - Saline, G-2- L-Ala-Gln, G-3-control (Sham). G-1 and G-3 groups were treated with saline 2.0 ml or L-Ala-Gln (0.75mg/Kg) intraperitoneally (ip) respectively, 2 hours before laparotomy. Anesthetized rats were subjected to laparotomy and total hepatic ischemia (30 minutes) induced by by clamping of portal triad. Control group underwent peritoneal puncture, two hours before the sham operation (laparotomy only). At the end of ischemia (G1 and G2), the liver was reperfused for 60 minutes. Following reperfusion blood samples were collected for evaluation of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels. Liver (medium lobe) was removed for immunohistochemistry study with antibody for Caspase-3. RESULTS: It was found a significant decrease (p<0.05) of ALT levels (270.6 +40.8 vs 83.3 +5.5 - p <0.05), LDH (2079.0 +262.4 vs. 206.6 +16.2 - p <0.05) and Caspase-3 expression (6.72 +1.35 vs. 2.19 +1.14, p <0.05) in rats subjected to I / R, comparing the group treated with L-Ala -Gln with G-2. Also, the ALT level was significantly lower (P<0.05) in G-1 and G-2 groups than in G-3 (control group). CONCLUSION: L-Ala-Gln preconditioning in rats submitted to hepatic I/R significantly reduces ALT, LDH and Caspase-3 expression, suggesting hepatic protection.


Author(s):  
Alberto Calleri ◽  
Dorotea Roggio ◽  
Victor Navarro-Tableros ◽  
Nicola De Stefano ◽  
Chiara Pasquino ◽  
...  

AbstractHepatic ischemia-reperfusion injury (IRI) is observed in liver transplantation and hepato-biliary surgery and is associated with an inflammatory response. Human liver stem cell-derived extracellular vesicles (HLSC-EV) have been demonstrated to reduce liver damage in different experimental settings by accelerating regeneration and by modulating inflammation. The aim of the present study was to investigate whether HLSC-EV may protect liver from IRI in a mouse experimental model. Segmental IRI was obtained by selective clamping of intrahepatic pedicles for 90 min followed by 6 h of reperfusion. HLSC-EV were administered intravenously at the end of the ischemic period and histopathological and biochemical alterations were evaluated in comparison with controls injected with vehicle alone. Intra liver localization of labeled HLSC-EV was assessed by in in vivo Imaging System (IVIS) and the internalization into hepatocytes was confirmed by fluorescence analyses. As compared to the control group, administration of 3 × 109 particles (EV1 group) significantly reduced alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) release, necrosis extension and cytokines expression (TNF-α, CCL-2 and CXCL-10). However, the administration of an increased dose of HLSC-EV (7.5 × 109 particles, EV2 group) showed no significant improvement in respect to controls at enzyme and histology levels, despite a significantly lower cytokine expression. In conclusion, this study demonstrated that 3 × 109 HLSC-EV were able to modulate hepatic IRI by preserving tissue integrity and by reducing transaminases release and inflammatory cytokines expression. By contrast, a higher dose was ineffective suggesting a restricted window of biological activity.


2002 ◽  
Vol 282 (6) ◽  
pp. G962-G971 ◽  
Author(s):  
Hiroshi Uchinami ◽  
Yuzo Yamamoto ◽  
Makoto Kume ◽  
Kei Yonezawa ◽  
Yasuhide Ishikawa ◽  
...  

Hepatic ischemia-reperfusion (I/R) injury continues to be a fatal complication after liver surgery. Heat shock (HS) preconditioning is an effective strategy for protecting the liver from I/R injury, but its exact mechanism is still unclear. Because the activation of nuclear factor-κB (NF-κB) is an important event in the hepatic I/R-induced inflammatory response, the effect of HS preconditioning on the pathway for NF-κB activation was investigated. In the control group, NF-κB was activated 60 min after reperfusion, but this activation was suppressed in the HS group. Messenger RNA expressions of proinflammatory mediators during reperfusion were also reduced with HS preconditioning. Concomitant with NF-κB activation, NF-κB inhibitor I-κB proteins were degraded in the control group, but this degradation was suppressed in the HS group. This study shows that HS preconditioning protected the liver from I/R injury by suppressing the activation of NF-κB and the subsequent expression of proinflammatory mediators through the stabilization of I-κB proteins.


2020 ◽  
Vol 21 (11) ◽  
pp. 4106
Author(s):  
Natalie Chaves Cayuela ◽  
Marcia Kiyomi Koike ◽  
Jacqueline de Fátima Jacysyn ◽  
Roberto Rasslan ◽  
Anderson Romério Azevedo Cerqueira ◽  
...  

N-acetylcysteine (NAC) is a pharmacological alternative with great potential for reducing the deleterious effects of surgical procedures on patients with steatohepatitis. We evaluated the effect of NAC on hepatic ischemia/reperfusion (I/R) injury in C57BL/6J mice, 8 weeks-old, weighing 25–30 g, with steatohepatitis induced by a methionine- and choline-deficient (MCD) diet. Groups: MCD group (steatohepatitis), MCD-I/R group (steatohepatitis plus 30 min of 70% liver ischemia and 24 h of reperfusion), MCD-I/R+NAC group (same as MCD-I/R group plus 150 mg/kg NAC 15 min before ischemia), and control group (normal AIN-93M diet). Liver enzymes and histopathology; nitrite and TBARS (thiobarbituric acid reactive substances) levels; pro-inflammatory cytokines; antioxidants enzymes; Nrf2 (nuclear factor erythroid-2-related factor 2) expression; and apoptosis were evaluated. In the group treated with NAC, reductions in inflammatory infiltration; AST (aspartate aminotransferase), nitrite, and TBARS levels; GPx (gutathione peroxidase) activity; cytokines synthesis; and number of apoptotic cells were observed while the GR (glutathione reductase) activity was increased. No differences were observed in Nfr2 expression or in SOD (superoxide dismutase), CAT (catalase), and GST (glutathione S-transferase) activities. Thus, it may be concluded that NAC exerts beneficial effects on mice livers with steatohepatitis submitted to I/R by reducing oxidative stress, inflammatory response, and cell death.


2018 ◽  
Vol 9 (2) ◽  
pp. 33-43
Author(s):  
Jeovana Pinheiro Fernandes de Souza ◽  
Juliana Mendonça Freire ◽  
Italo Medeiros Azevedo ◽  
Fabio Medeiros de Azevedo ◽  
Artur Da Silva Carriço ◽  
...  

Purpose: To evaluate the effect of hydration with simple Ringer's solution submitted to magnetic field in rats under renal ischemia and reperfusion (I/R) model, using biochemical and histopathological evaluation. Methods: Wistar rats were allocated into 2 equal groups of 6 animals each: Renal ischemia/reperfusion group + hydration with magnetic Ringer (mag Ringer).  The left kidney underwent ischemia for 30 minutes. The right kidney was not manipulated. Thereafter, i.v. hydration was performed with 3 ml mag Ringer; Group renal I/R + hidration with simple Ringer. The simple Ringer solution was submitted to a magnetic field of 20mT intensity for 2 hours immediately prior to the surgical procedure. After 24 hours, under anesthesia blood was collected for dosing serum urea and creatinine. Histopathological analysis was performed on the left kidney (HE staining). Results: There was no significant difference between the creatinine (p=0.764) and urea (p = 0.926) values ​​between the control and test groups (non-parametric Mann-Whitney test). Comparing the histopathological scores, there was a significant difference between the groups, with higher levels of lesions in the mag Ringer treated group (p=0.025) - Mann-Whitney test. Conclusion: The use of Ringer's solution submitted to magnetic field for intravenous hydration in a renal ischemia/reperfusion model did not alter the renal function and had a negative influence on the histopathological findings on the kidney, when compared to control.


2021 ◽  
Author(s):  
Hang Li ◽  
Jilang Tang ◽  
Weiqi Zhang ◽  
Liping Ai ◽  
Shixia Zhang

Abstract Background: Hepatic ischemia-reperfusion injury (IRI) remains a major complication of liver surgery, dexmedetomidine (DEX) has a certain protective effect on liver during ischemia-reperfusion, but the underlying mechanisms are not fully understood. This study explored the protective effects of DEX and investigated whether DEX protects against hepatic IRI by inhibiting endoplasmic reticulum stress (ERS) and its downstream apoptotic pathway in a rat model. Methods: Thirty-six male Sprague-Dawley (SD) rats were divided into six groups: S, IR, DL, DM1, DH and DM2 group. Group S was subjected to laparotomy, and exposure of the portal triad without occlusion. I-R injury model was induced by clamping the portal vessels supplying the middle and left hepatic lobes for 30 min in IR, DL, DM1, DH and DM2 group. Then DL, DM1, DH group received DEX of 25 μg/kg, 50 μg/kg and 100 μg/kg intraperitoneally at 30 min before ischemia, respectively, DM2 group received 50 μg/kg DEX intraperitoneally 30 min after reperfusion, and IR group received normal saline. After 6 h of reperfusion, assessment of liver function, histopathology, oxidative stress was performed. The liver cell microstructure was detected by transmission electron microscopy. Hepatocyte apoptosis was determined by TUNEL assay. Real-time PCR, Western blotting were performed to analyze various ERS molecules. Results: We observed that DEX protected the liver by alleviating hepatocytes damage, reducing the content of ALT and MDA, increasing the activity of SOD, reducing the number of TUNEL-positive cells, down-regulating the expression of GRP-78, PERK, ATF-6, Caspase-12 mRNA, and p-PERK, p-IRE-1 α, CHOP proteins, up-regulating Bcl-2 protein. The effect of 50 μg/kg DEX is superior to 25 μg/kg DEX, but not significantly different from 100μg/kg DEX. There was no significant difference in the above monitoring indexes between DM1 and DM2 group. Conclusions: DEX protects the liver from IRI by inhibiting ERS and cell apoptosis. The protective effect of DEX was dose-dependent in a certain dose range, both DEX administered prior to ischemia and following reperfusion markedly reduced liver injury induced by hepatic IRI in mice.


PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11909
Author(s):  
Yitong Pan ◽  
Shuna Yu ◽  
Jianxin Wang ◽  
Wanzhen Li ◽  
Huiting Li ◽  
...  

The aim of this study was to investigate the changes of TLR4/NLRP3 signal during hepatic ischemia-reperfusion injury (HIRI) and to verify whether N-acetyl-L-tryptophan (L-NAT) protected hepatocytes by regulating the activation of TLR4/NLRP3 signal. We have established the rat HIRI model and H2O2-induced cell damage model to simulate ischemia-reperfusion injury and detect the corresponding indicators. Compared with the sham group, Suzuki score and the level of serum ALT increased after HIRI, accompanied by an increased expression of NLRP3, ASC, Caspase-1, IL-1β, TLR4, and NF-κB. While L-NAT pretreatment reversed the above-mentioned changes. Compared with the control group, cells in the H2O2 treated group became smaller in cell volume and round in shape with unclear boundaries. Similar to the phenotypes in vivo, H2O2 treatment also induced significant increase in expression of pyroptosis-related proteins (NLRP3, ASC, Caspase-1 and IL-1β) and inflammatory factors (TLR4 and NF-κB). While L-NAT pretreatment attenuated injuries caused by H2O2. In conclusion, the present findings demonstrate that L-NAT alleviates HIRI by regulating activation of NLRP3 inflammasome, which may be related to the TLR4/NF-κB signaling pathway.


2020 ◽  
Author(s):  
Yajun Ma ◽  
Zhihui Jiao ◽  
Xiaoning Liu ◽  
Qianzhen Zhang ◽  
Chenxi Piao ◽  
...  

Abstract Background: The therapeutic effects of adipose-derived mesenchymal stem cells (ADSCs) may mainly come from their paracrine effects. ADSCs can ameliorate hepatic ischemia-reperfusion injury (IRI). We explored the therapeutic effect of ADSCs secretome from the perspective of excessive autophagy of hepatocytes induced by hepatic IRI.Methods: In this study, we established a miniature pig model of hepatic ischemia-reperfusion (I/R) combined with hepatectomy using laparoscopic technique, and transplanted ADSCs and adipose-derived mesenchymal stem cell-conditioned medium (ADSC-CM) into the liver parenchyma immediately after surgery. Histopathological and TEM examinations were performed on liver tissue samples collected. We analyzed the roles of ADSC-CM and ADSCs in autophagy by RT-qPCR, western-blot and immunohistochemistry. Results: The results showed that ADSCs and ADSC-CM all alleviated the pathological changes of liver tissue and the microstructural damage of hepatocytes after IRI. Moreover, the expression of the critical markers of autophagy including Beclin-1, ATG5, ATG12 and LC3II all decreased, whereas expression of p62 increased. And the data of autophagy regulation between ADSC-CM and ADSCs showed no significant difference. Finally, we found that ADSC-CM possibly inhibited autophagy by regulating the PI3K/Akt/mTOR pathway.Conclusion: ADSC-CM can ameliorate excessive autophagy injury in hepatic I/R combined with partial hepatectomy, which is possibly involved with the modulation of the PI3K/Akt/mTOR signaling pathway. There was no significant difference between ADSCs and ADSC-CM in the regulation of hepatocyte autophagy. Therefore, ADSCs may improve the excessive autophagy injury of hepatocytes in hepatic I/R combined with hepatectomy through paracrine effect, thus protecting the liver and promoting the liver tissue repair.


2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 32-37 ◽  
Author(s):  
Petrúcia Maria Antero Pinheiro ◽  
Ana Paula Bomfim Soares Campelo ◽  
Sérgio Botelho Guimarães ◽  
Régia Maria Vidal do Patrocínio ◽  
José Telmo Valença Junior ◽  
...  

PURPOSE: This study aimed to assess the effects of preconditioning with mixtures of oils containing high/low ratio of ω-6/ω-3 and ω-9/ω-6, respectively, in an experimental model of cerebral ischemia-reperfusion (I/R). METHODS: Forty-two Wistar rats were randomly distributed into two groups: control (n=24) and test (n=18). Control group was subdivided in 4 subgroups (n=6): G1: Sham-Water; G2: I/R-Water; G3: Sham-Isolipidic and G4: I/R-Isolipid. The animals received water or a isolipid mixture containing ω-3 oils (8:1 ratio) and ω-9/ω-6 (0.4:1 ratio) by gavage for seven days. Test group included 3 subgroups (n=6) G5: I/R-Mix1, G: 6 I/R-Mix2 and G7: I/R-Mix3. Test group animals received oily mixtures of ω-3 (1.4:1 ratio) and ω-6 (3.4:1 ratio), differing only in source of ω-3: G5 (alpha-linolenic acid); G6 (alpha-linolenic, docosahexaenoic and eicosapentaenoic acids), and G7 (alpha-linolenic and docosahexaenoic acids). On day 7 I/R rats underwent cerebral ischemia with bilateral occlusion of common carotid arteries for 1 hour followed by reperfusion for 3 hours. G1 and G3 animals underwent sham operation. Concluded the experiment, animals were decapitated and their brains sliced for red neurons (RN) count in CA3 area of the hippocampus. Variables were compared using ANOVA-Tukey test. RESULTS: The use of different mix preparations promoted a decrease in red cell count in all three groups (G5/G6/G7), compared with G2/G4, confirming the protective effect of different oil blends, regardless of ω-3 source. CONCLUSION: Pre-conditioning with mixtures of oils containing high ratio ω-6/ω-3 and low ω-9/ω-6 relationship protects brain neurons against I/R injury in an experimental model.


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