5-lipoxygenase activation is involved in the mechanisms of chronic hepatic injury in a rat model of chronic aluminum overload exposure

Mai, Shaoshan; He, Qin; Wang, Hong; Hu, Xinyue; Luo, Ying; Yang, Yang; Kuang, Shengnan; Tian, Xia; Ma, Jie; Yang, Jing

doi:10.1016/j.taap.2016.06.029

Cited by 17 publications

(17 citation statements)

References 33 publications

(3 reference statements)

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“…Meloxicam was purchased from Kunshan Rotam Reddy Pharmaceutical Co., Ltd, China. According to previously reported methods [13, 17], an aluminium gluconate solution (20 mg Al 3+ ·ml −1 ) was prepared on the day of the experiments by adding 17.9 g of AlCl 3 · 6H 2 O and 9.9 g of sodium gluconate to 100 ml of double distilled water (ddH 2 O), and the pH of the solution was adjusted to approximately 6.0.…”

Section: Methodsmentioning

confidence: 99%

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The protection of meloxicam against chronic aluminium overload-induced liver injury in rats

Yang

Wang

et al. 2017

Oncotarget

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Section: Methodsmentioning

confidence: 99%

“…5-lipoxygenase is a metabolic pathway of AA to produce LTs. Our previous research showed that 5-lipoxygenase inhibitors could significantly alleviate inflammation and oxidative stress in chronic Al-overload liver injury [17]. However, cyclooxygenase (COX) pathway is an another very important metabolic pathway of AA.…”

Section: Introductionmentioning

confidence: 99%

The protection of meloxicam against chronic aluminium overload-induced liver injury in rats

Yang

Wang

et al. 2017

Oncotarget

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“…The expression of COX‐2 and 5‐LOX increased in chronic aluminum‐loaded liver injury after intervention with COX‐2 inhibitor and 5‐LOX inhibitor, respectively. The expressions of COX‐2 and 5‐LOX were significantly reduced, respectively . However, whether intervention with COX‐2 inhibitor can lead to the compensation of 5‐LOX pathway and vice versa is not clear in chronic aluminum‐loaded liver injury rat.…”

Section: Introductionmentioning

confidence: 96%

Treatment with either COX‐2 inhibitor or 5‐LOX inhibitor causes no compensation between COX‐2 pathway and 5‐LOX pathway in chronic aluminum overload‐induced liver injury in rats

Xia

Wang

et al. 2019

Fundamemntal Clinical Pharma

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This study was designed to observe the compensation between cyclooxygenase‐2 pathway and 5‐lipoxygenase pathway in chronic aluminum overload‐induced liver injury rats. A rat hepatic injury model of chronic aluminum injury was established by the intragastric administration of aluminum gluconate (Al3 + 200 mg/kg per day, 5 days a week for 20 weeks). The COX‐2 inhibitor [meloxicam (1 mg/kg)] and 5‐LOX inhibitor [caffeic acid (30 mg/kg)] were intragastrically administered 1 h after aluminum administration. The histopathology was detected by hematoxylin‐eosin staining. A series of biochemical indicators were measured with biochemistry assay or ELISAs. The expressions of COX‐2 and 5‐LOX were measured by immunohistochemistry. Our experimental results showed that aluminum overload caused a significant damage to the liver and also significantly increased the expressions of COX‐2, 5‐LOX and the levels of inflammation and oxidative stress. The administration of meloxicam and caffeic acid significantly protected livers against histopathological injury, significantly decreased plasma ALT, AST, and ALP levels, significantly decreased TNF‐α, IL‐6, IL‐1β levels, and oxidative stress. However, the administration of caffeic acid did not significantly increase the expression of COX‐2 compared with the model group. On the other hand, the administration of meloxicam also did not significantly increase the expression of 5‐LOX compared with the model group. Our results indicate that there is no compensation between COX‐2 pathway and 5‐LOX pathway by inhibiting either COX‐2 or 5‐LOX in chronic aluminum overload‐induced liver injury rat.

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“…High levels of aluminium pose many health risks and have been implicated in the aetiology of different neurodegenerative diseases including dialysis encephalopathy, Alzheimer's disease, and Parkinson's disease . Moreover, aluminium can induce liver injury by triggering reactive oxygen species/antioxidant imbalance, lipid peroxidation, inflammatory cascades, and apoptosis …”

Section: Introductionmentioning

confidence: 99%

“…7 Moreover, aluminium can induce liver injury by triggering reactive oxygen species/antioxidant imbalance, lipid peroxidation, inflammatory cascades, and apoptosis. 8,9 A growing body of evidence suggests a link between insulin resistance (IR), a core component of metabolic syndrome, and liver disorders. IR plays an essential role in the pathogenesis and the progression of non-alcoholic fatty liver disease (NAFLD), 10 which can further progress to steatohepatitis and other serious complications including cirrhosis and hepatocellular carcinoma.…”

mentioning

confidence: 99%

The concurrent exposure to aluminium and fructose induces liver injury in rats: Protection by monoammonium glycyrrhizinate

Zakaria

Hasan

Mahmoud

et al. 2020

Clin Exp Pharma Physio

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Aluminium is a ubiquitous element that occurs naturally in the soil making human exposure to it unavoidable. It is implicated in the aetiology of different neurodegenerative diseases and can induce liver injury. In addition, insulin resistance (IR) plays an essential role in the pathogenesis and the progression of liver disorders. The increased consumption of fructose contained in soft drinks and western pattern diet results in IR that along with the wide distribution of aluminium make the concurrent exposure conceivable and increase the risk of liver injury. Therefore, the present study explores the hepatotoxic effects of aluminium and fructose administered concurrently and evaluates the possible protection by monoammonium glycyrrhizinate (MAG). Liver injury was induced by the administration of aluminium chloride (34 mg/kg/d) plus 10% (w/v) fructose in drinking water. Male rats were treated with either MAG (40 mg/kg/d) or silymarin (SIL, 100 mg/kg/d). The concurrent administration of aluminium and fructose (FRUAL) induced liver injury manifested as a significant elevation of serum liver enzymes activities, bilirubin level, and prothrombin time, as well as reduction of albumin level. On the other hand, the administration of MAG improved the FRUAL‐induced aberrations of liver function tests and hepatic cytoarchitecture. We assume that the MAG‐induced suppression of oxidative stress, toll‐like receptor 4 pathway activation, inflammation, and apoptosis might play a crucial role in the hepatoprotective effect of MAG in this model. Intriguingly, the hepatoprotective effect MAG against FRUAL‐induced liver injury surpasses that of the gold standard SIL, suggesting MAG as a better alternative to SIL.

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5-lipoxygenase activation is involved in the mechanisms of chronic hepatic injury in a rat model of chronic aluminum overload exposure

Cited by 17 publications

References 33 publications

The protection of meloxicam against chronic aluminium overload-induced liver injury in rats

The protection of meloxicam against chronic aluminium overload-induced liver injury in rats

Treatment with either COX‐2 inhibitor or 5‐LOX inhibitor causes no compensation between COX‐2 pathway and 5‐LOX pathway in chronic aluminum overload‐induced liver injury in rats

The concurrent exposure to aluminium and fructose induces liver injury in rats: Protection by monoammonium glycyrrhizinate

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