Salutary Effects of Cepharanthine against Skeletal Muscle and Kidney Injuries following Limb Ischemia/Reperfusion

Kao, Ming‐Chien; Chung, C.‐S.; Chang, Ya Ying; Lin, Chih Kung; Sheu, Joen Rong; Huang, Chun Jen

doi:10.1155/2015/504061

Cited by 11 publications

(10 citation statements)

References 37 publications

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“…The freshly harvested caudate lobe was weighed and placed in the oven at 80 °C for 24 h and then weighed again. The wet/dry weight ratio was then calculated [ 46 ].…”

Section: Methodsmentioning

confidence: 99%

Peptide-Based TNF-α-Binding Decoy Therapy Mitigates Lipopolysaccharide-Induced Liver Injury in Mice

et al. 2020

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A peptide named SEM18, possessing structural similarity to the binding site of tumor necrosis factor (TNF)-α to TNF receptor 1 (TNFR1), was designed. We investigated whether the SEM18 peptide can mitigate lipopolysaccharide (LPS)-induced liver injury in mice. Adult male Balb/cJ mice received LPS (15 mg/kg; LPS group) or LPS plus SEM18 (LSEM group). Control groups were run simultaneously. At 2 h after LPS, the first dose of SEM18 (0.3 mg/kg) was administered, followed by three supplemental doses of SEM18 (0.15 mg/kg, every 2 h). At 24 h after LPS, surviving mice were euthanized for analyses. Compared with the LPS group, binding of TNF-α to TNFR1 in liver tissues was significantly lower in the LSEM group (p < 0.001). Plasma concentrations of aspartate transaminase and alanine transaminase, as well as Suzuki’s scores (liver damage assessment), wet/dry weight ratios, levels of polymorphonuclear neutrophil infiltration, and levels of mitochondrial injury in liver tissues, of the LSEM group were significantly lower than in the LPS group (all p < 0.05). Levels of necroptosis, pyroptosis, apoptosis, and autophagy upregulation in liver tissues in the LSEM group were also significantly lower than in the LPS group (all p < 0.05). Notably, exogenous TNF-α counteracted these effects of SEM18. SEM18 peptide mitigates LPS-induced liver injury in mice.

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“…The freshly harvested caudate lobe was weighed and placed in the oven at 80 °C for 24 h and then weighed again. The wet/dry weight ratio was then calculated [ 46 ].…”

Section: Methodsmentioning

confidence: 99%

Peptide-Based TNF-α-Binding Decoy Therapy Mitigates Lipopolysaccharide-Induced Liver Injury in Mice

et al. 2020

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“…Currently, many treatment procedures and medications for preventing and ameliorating kidney injury induced by limb I/R are being developed [ 18 , 19 ]. Ischemic postconditioning (I-postC) is a promising method to alleviate remote organ dysfunction by performing several cycles of transient ischemia and reperfusion intervention on the ischemic limb.…”

Section: Introductionmentioning

confidence: 99%

Ischemic postconditioning ameliorates acute kidney injury induced by limb ischemia/reperfusion via transforming TLR4 and NF-κB signaling in rats

et al. 2021

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Background The present study investigated the influence of ischemic postconditioning (I-postC) on the adjustment of renal injury after limb ischemia-reperfusion (I/R) injury, to elucidate the mechanisms of the Toll-like receptor 4 (TLR 4)/NF-κB signaling pathway using histopathological and immunohistochemical methods. Methods Male Sprague-Dawley rats were randomly assigned to five groups (numbered from 1 to 5): the sham group (Group 1, only the anesthesia procedure was conducted without limb I/R), the I/R group (Group 2, 4 h of reperfusion was conducted following 4 h limb ischemia under anesthesia), the I/R + I-postC group (Group 3, 4 h of ischemia and 4 h of reperfusion was conducted; before perfusion, 5 min of limb ischemia and 5 min of reperfusion were performed in the rats and repeated 3 times), the I/R + TAK group (Group 4, rats were injected with TLR4 antagonist TAK through the caudal vein before limb ischemia and reperfusion under anesthesia), the TAK group (Group 5, rats were injected with TAK, and the anesthesia procedure was conducted without limb I/R). Histological changes in the kidney in different groups were observed, and the extent of tubular injury was assessed. Changes in biochemical indexes and the expression of inflammatory factors, TLR4, and NF-κB were also evaluated. Results Compared with rats in the I/R group, the secretion of inflammatory factors and the expression levels of TLR4 and NF-κB were decreased in rats in the I/R + I-postC group. Histological analysis revealed renal injury, including inflammatory cell infiltration, dilatation of the tubuli lumen, congestion in glomerular capillaries, degeneration of tubuli epithelial cells, and necrosis was ameliorated by I-postC. Immunohistochemical studies showed that I/R-induced elevation in TLR4 and NF-κB expression was reduced by I-postC treatment. Moreover, the expression levels of TLR4, NF-κB, and inflammatory factors in rats in the I/R + TAK group were also decreased, and the renal pathological lesion was alleviated, which was similar to that in rats in the I/R + I-postC group. Conclusions The present findings suggest that I-postC can reduce tissue injury and kidney inflammation induced by limb I/R injury, possibly via inhibition of the TLR4 and NF-κB pathways.

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“…Similarly, a previous research also showed that limb ischemia suffered by mice for 2 h, then followed by reperfusion can cause injury to their lungs, but not in their liver and kidneys [ 13 ]. Unlike in the previous research, other researchers have also shown that limb ischemia suffered by mice for 3 h, then followed by reperfusion can cause injury to their lungs and kidneys, as well as the muscle of their lower limb [ 14 , 15 ].…”

Section: Discussionmentioning

confidence: 99%

Effects of hyperbaric therapy on liver morphofunctional of rabbits (Oryctolagus cuniculus) after hind limb ischemia-reperfusion injury

2017

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Aim:The objective of this research was to study and to prove the effectiveness of hyperbaric oxygen therapy (HBOT) starting time on liver morphofunctional changes after ischemia-reperfusion in the hind limb of rabbits.Materials and Methods:This research used a complete randomized design with 4 groups and 6 repetitions on each. After 6 h artery femoral is ligation, reperfusion was performed for 100 min (G1), HBOT for 90 min after 10 min reperfusion (G2), 10 min reperfusion (G3), and HBOT 90 min after 60 min reperfusion (G4). Then, all of the rabbits were sacrificed. The liver and blood were taken for histopathological changes examination as well as for measuring the level of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The statistical test using Kruskal–Wallis and Mann–Whitney showed that the score of degeneration, necrosis, and portal inflammation in groups without HBOT (G1 and G3) were not significantly different, as well as in group with HBOT (G2 and G4) (p>0.05). However, the scores of histopathological changes in G1 and G3 were significantly different from those in G2 and G4 (p<0.05). The levels of AST and ALT in the groups without hyperbaric therapy (G1 and G3) were not significantly different from those in the groups treated with hyperbaric therapy (G2 and G4) (p>0.05).Result::Hind limb ischemia injury reperfusion can trigger damage for liver morphology, but not lead to liver dysfunction. Reperfusion can trigger increased activity of neutrophils, while neutrophil infiltration in the organ will lead to dysfunction. HBOT can inhibit the activity of neutrophils and the dysfunction of organs caused by ischemic reperfusion.Conclusion:HBOT for 90 min, both 10 and 60 min after the reperfusion, can protect hepatocytes from damage.

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Salutary Effects of Cepharanthine against Skeletal Muscle and Kidney Injuries following Limb Ischemia/Reperfusion

Cited by 11 publications

References 37 publications

Peptide-Based TNF-α-Binding Decoy Therapy Mitigates Lipopolysaccharide-Induced Liver Injury in Mice

Peptide-Based TNF-α-Binding Decoy Therapy Mitigates Lipopolysaccharide-Induced Liver Injury in Mice

Ischemic postconditioning ameliorates acute kidney injury induced by limb ischemia/reperfusion via transforming TLR4 and NF-κB signaling in rats

Effects of hyperbaric therapy on liver morphofunctional of rabbits (Oryctolagus cuniculus) after hind limb ischemia-reperfusion injury

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