Diacerein protects rats with liver ischemia/reperfusion damage: Down-regulation of TLR4/ NFκ-B signaling pathway

Ibrahim, Mohamed; Abdelzaher, Walaa Yehia; Ibrahim, Yasmine; Ahmed, Ashraf; Welson, Nermeen N.; Al-Rashed, Sarah; Batiha, Gaber El‐Saber; Abdel-Aziz, Asmaa Mohamed

doi:10.1016/j.biopha.2020.111063

Cited by 27 publications

(26 citation statements)

References 32 publications

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“…They can recognize and interact with certain molecular proteins of host apoptosis surfaces. TLR4 is a cornerstone in initiating the inflammatory response via stimulation of Hsp70 in acute injuries as MI and mediating the release of pro-inflammatory cytokines as TNF-α and IL-1β via the stimulation of NF-κB; the nuclear transcription agent ( Tao et al, 2016 ; Ibrahim et al, 2021 ). This comes in line with the present results of the significant increase of cardiac TLR4 in MI.…”

Section: Discussionmentioning

confidence: 99%

“…Toll-like receptor 4 (TLR4), a member of the transmembrane recognition proteins family, is essential for the stimulation of inflammation noticed in experimental ischemia/reperfusion (I/R). Activation of TLR4 ultimately stimulates the pro-inflammatory cytokines release e.g., tumor necrosis factor-α (TNF-α) and interleukins-1β (IL-1β) ( Ibrahim et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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Dapsone Ameliorates Isoproterenol-Induced Myocardial Infarction via Nrf2/ HO-1; TLR4/ TNF-α Signaling Pathways and the Suppression of Oxidative Stress, Inflammation, and Apoptosis in Rats

et al. 2021

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Myocardial infarction (MI) is a critical condition that can happen with high doses or rapid termination of beta blockers therapy. The study aimed to evaluate the potential anti-toxic value of DAP against isoproterenol (ISO) - induced MI. Twenty-eight male Wistar rats were used for the study. The rodents were assigned to four groups (n = 7) and the treatments were given for 12 days as follows; Group 1 (control): were administrated normal saline, Group 2 (DAP control): were administrated DAP (10 mg/kg/day IP), Group 3 (ISO group): were administrated ISO (100 mg/kg, IP on the 11th and 12th days of the experiment), and Group 4 (DAP + ISO): co-treated with DAP plus ISO. The measured parameters were cardiac malondialdehyde (MDA), reduced glutathione (GSH), total nitrite/nitrate (NOx), catalase (CAT), serum cardiac biomarkers; CK-MB, ALT, LDH, and ALK-PH. Also, interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase-1 (HO-1), toll-like receptor 4 (TLR4), caspase-3 activity, and hepatic BAX and Bcl-2 were also assessed. Also, histological examination and vimentin immuno-expressions were studied. ISO group exhibited MI as evidenced by the elevation in serum cardiac biomarkers, MDA, NOx, IL-1β, TNF-α, and caspase-3 together with the reduction in GSH, Nrf2, HO-1 levels, and a faint vimentin immuno-reaction. Histological alterations revealing distorted cardiomyocytes; vacuolation, edema, pyknosis, and fragmentation were also noticed. DAP significantly ameliorated all the examined toxicity indicators. DAP revealed efficient ameliorative actions against ISO-caused MI by marked reduction in myocardial infarct size and suppressed oxidative stress, inflammation, and apoptosis via the up-regulation of the Nrf2/HO-1; TLR4/TNF-α signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dapsone Ameliorates Isoproterenol-Induced Myocardial Infarction via Nrf2/ HO-1; TLR4/ TNF-α Signaling Pathways and the Suppression of Oxidative Stress, Inflammation, and Apoptosis in Rats

et al. 2021

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“…Any obstruction in blood flow and reperfusion of blood flow after removing the obstacle causes tissue damage in the intestine (2,3). Various conditions and diseases cause ischemia-reperfusion in this artery (4,5). These include a trapped hernia.…”

Section: Introductionmentioning

confidence: 99%

“…These include a trapped hernia. Ischemia-reperfusion damage consists of a sequence of chemical events that lead to cell dysfunction and necrosis and consists of two parts (5). Direct damage (which is a mild injury that occurs during the ischemic phase, the tissue and the organ are deprived of blood and they receive insufficient nutrients and oxygen.)…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of melatonin as an antioxidant in the intestine of rats with superior mesenteric arterial occlusion

Yuan

Zhang

2022

Cell Mol Biol (Noisy-le-grand)

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The superior mesenteric artery is a branch of the aortic artery that supplies blood to the small and some parts of the large intestine. Any obstruction in blood flow and reperfusion causes tissue damage in the intestine. This study aimed to determine the rate of fat peroxidation and tissue protein as an indicator of tissue degradation after ischemia and reperfusion following induction of superior mesenteric artery occlusion in the intestine and to evaluate the protective effect of melatonin as a free radical scavenger and antioxidants in rats. In this study, 36 male Wistar-Albino rats weighing between 80-120 g were equally divided into six groups and received different melatonin doses (10, 20, and 30 mg/kg) intramuscularly. In this regard, Group 1 was the control group, Group 2 was the Sham group (underwent surgery to dissect the upper mesenteric artery and injected the same volume of solvent), Group 3 was Ischemia-reperfusion (IR), Group 4 was IR with melatonin at a dose of 10 mg/kg, Group 5 was IR with melatonin at a dose of 20 mg/kg, and Group 6 was IR with melatonin at a dose of 30 mg/kg. The results showed that the level of tissue malondialdehyde (MDA) was significantly lower in groups 4, 5, and 6 than in group 3 (P <0.05). Tissue protein levels were significantly higher in group 4 than in group 3 (P <0.001). Tissue protein levels in groups 5 and 6 did not significantly differ from group 3 (P = 0.191). Overall, this study showed that melatonin at a dose of 10 mg/kg has an antioxidant effect preventing induced damage due to superior mesenteric artery occlusion.

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Targeting PI3K/p‐Akt/eNOS, Nrf2/HO‐1, and NF‐κB/p53 signaling pathways by angiotensin 1–7 protects against liver injury induced by ischemia–reperfusion in rats

Ali,

Mohammed,

Hussein

et al. 2024

Cell Biochemistry & Function

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The liver is an important organ, and hepatic ischemia–reperfusion (IR) injury is a frequent pathophysiological process that can cause significant morbidity and mortality. Thus, our study aimed to investigate the effect of targeting PI3K/p‐Akt/eNOS (phosphoinositide 3‐kinase/phospho‐protein kinase B/endothelial nitric oxide synthase), Nrf2/HO‐1 (nuclear factor‐erythroid 2‐related factor‐2/heme oxygenase‐1), and NF‐κB/p53 (nuclear factor‐κB/tumor protein 53) signaling pathways by using angiotensin (1–7) [ang‐(1–7)] against hepatic injury induced by IR. Thirty‐two male rats were included in sham group, ang‐(1–7)‐treated group, hepatic IR group, and hepatic IR group treated with ang‐(1–7). The levels of hepatic ang‐(1–7), angiotensin II (Ang II), angiotensin‐converting enzyme 2 (ACE2), HO‐1, malondialdehyde (MDA), PI3K, and p‐Akt were assessed. The expressions of eNOS and B‐cell leukemia/lymphoma‐2 (BCL‐2) in the liver were determined. Histological assessment and immunohistochemical expression of NF‐κB, p53, and Nrf2 were carried out. The levels of reduced glutathione (GSH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), tumor necrosis factor‐α (TNF‐α), and interleukin‐6 (IL‐6) in serum were estimated. Results showed that administration of ang‐(1–7) to hepatic IR rats led to significant amelioration of hepatic damage through a histological evaluation that was associated with significant upregulation of the expressions of PI3K/p‐Akt/eNOS and Nrf2/HO‐1 with downregulation of NF‐κB/p53 signaling pathways. In conclusion, PI3K/p‐Akt/eNOS and Nrf2/HO‐1 signaling pathways are involved in the protective effects of ang‐(1–7) against hepatic damage induced by IR. Therefore, ang‐(1–7) can be used to prevent hepatic IR, which occurs in certain conditions such as liver transplantation, hemorrhagic shock, and severe infection.

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Diacerein protects rats with liver ischemia/reperfusion damage: Down-regulation of TLR4/ NFκ-B signaling pathway

Cited by 27 publications

References 32 publications

Dapsone Ameliorates Isoproterenol-Induced Myocardial Infarction via Nrf2/ HO-1; TLR4/ TNF-α Signaling Pathways and the Suppression of Oxidative Stress, Inflammation, and Apoptosis in Rats

Dapsone Ameliorates Isoproterenol-Induced Myocardial Infarction via Nrf2/ HO-1; TLR4/ TNF-α Signaling Pathways and the Suppression of Oxidative Stress, Inflammation, and Apoptosis in Rats

Protective effect of melatonin as an antioxidant in the intestine of rats with superior mesenteric arterial occlusion

Targeting PI3K/p‐Akt/eNOS, Nrf2/HO‐1, and NF‐κB/p53 signaling pathways by angiotensin 1–7 protects against liver injury induced by ischemia–reperfusion in rats

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