Sequential changes of connexin32 and connexin26 in ischemia-reperfusion of the liver in rats

Nakashima, Yuichi; Kohno, Hitoshi; El-Assal, Osama N.; Dhar, Dipok Kumar; Ono, Takashi; Yamanoi, Akira; Nagasue, Naofumi

doi:10.1016/s1386-6346(03)00188-8

Cited by 10 publications

(7 citation statements)

References 29 publications

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“…In later phases, deterioration of connexin production was noticed. Identical changes were seen in concentration of calcium, which is known to move intercellularly through gap junctions [66]. In a similar experimental model, it was found that the reductions in Cx32 mRNA and protein amounts occur at different time points and are driven by different posttranscriptional and posttranslational mechanisms in ischemic and non-ischemic liver areas during reperfusion [67].…”

Section: Gap Junctions In Liver Ischemia and Reperfusion Injurymentioning

confidence: 93%

Gap junctions and non-neoplastic liver disease

Vinken

2012

Journal of Hepatology

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Because of their critical role as goalkeepers of hepatic homeostasis, gap junctions are frequent targets in liver disease. This concept has been demonstrated on many occasions in the light of hepatocarcinogenesis. Relatively little focus has been put on the fate of gap junctions in other liver pathologies, including hepatitis, liver fibrosis and cirrhosis, cholestasis and hepatic ischemia and reperfusion injury. The present paper provides an in-depth description of the multiple changes in expression, localization and function of connexins, the molecular constituents of gap junctions. The use of connexins as biomarkers and therapeutic targets in liver disease is also illustrated.

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Section: Gap Junctions In Liver Ischemia and Reperfusion Injurymentioning

confidence: 93%

Gap junctions and non-neoplastic liver disease

Vinken

2012

Journal of Hepatology

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“…In animal models of hepatic ischaemia-reperfusion, an early decrease in Cx26 and Cx32 mRNA and protein expression was observed. 69,70 Partial prevention of this effect was obtained with actinomycin D, which prevents the degradation of Cx32 mRNA, although protein expression of Cxs remained low, suggesting that its regulation occurs by different posttranscriptional and post-translational mechanisms. 71 This alteration is likely to represent an adaptive response aimed at restricting the spread of noxious signals to healthy areas.…”

Section: Acute Liver Injury and Inflammationmentioning

confidence: 99%

Gap junctions in liver disease: Implications for pathogenesis and therapy

Hernández‐Guerra

Hadjihambi

Jalan

2019

Journal of Hepatology

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In the normal liver, cells interact closely through gap junctions. By providing a pathway for the trafficking of low molecular mass molecules, these channels contribute to tissue homeostasis and maintenance of hepatic function. Thus, dysfunction of gap junctions affects a wide variety of liver processes, such as differentiation, cell death, inflammation and fibrosis. In fact, dysfunctional gap junctions have been implicated, for more than a decade, in cholestatic disease, hepatic cancer and cirrhosis. Additionally, in recent years there is an increasing body of evidence that these channels are also involved in other relevant and prevalent liver pathological processes, such as non-alcoholic fatty liver disease, acute liver injury and portal hypertension. In parallel to these new clinical implications the available data include controversial observations. Thus, a comprehensive overview is required to better understand the functional complexity of these pores. This paper will review the most recent knowledge concerning gap junction dysfunction, with a special focus on the role of these channels in the pathogenesis of relevant clinical entities and on potential therapeutic targets that are amenable to modification by drugs.

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“…The segmental (70%) hepatic ischemia model was used in the present study (Nakashima et al, 2003;Saidi et al, 2015). A midline laparotomy was performed under anesthesia with 10% chloral hydrate (0.3 g/kg, i.p.)…”

Section: Induction Of Partial Hepatic Ischemiamentioning

confidence: 99%

Protective effects ofHammada scopariaflavonoid-enriched fraction on liver injury induced by warm ischemia/reperfusion

Saidi

Bourogâa

Bouaziz

et al. 2015

Pharmaceutical Biology

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Context: Hepatic ischemia/reperfusion injury (IRI) is a major cause of liver damage during liver surgery and transplantation. Plants have historically been used in treating liver damage, and Hammada scoparia (Pomel) (Chenopodiaceae) has been reported to possess a broad spectrum of pharmacological and therapeutic activities. Objective: In this study, a flavonoid-enriched fraction was used before the warm ischemia (WI) process as pharmacological preconditioning and in combination with technical postconditioning to evaluate their protective effects. Materials and methods: The rats were divided into five groups: a sham group; a control group (Control-IR) that was submitted to 60 min WI; a Pharmacological Preconditioning group (PreC-IR) that received flavonoid-enriched fraction (200 mg/kg body weight); a Postconditioning group (PostC) and a PreC + PostC group. Results: The use of the flavonoid-enriched fraction was noted to significantly (p50.05) reduce liver injury, as evidenced by the decrease in liver transaminase activities (AST and ALT) and lactic dehydrogenase (LDH), alkaline phosphatase (ALP), and lipid peroxidation (TBARS), levels as well as the enhancement of antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx)) responses. The results also indicated that, compared with the separate application of pharmacological preconditioning and postconditioning, the combination of both treatments was more effective in reducing tissue oxidative stress levels through modulating SOD, GSH-PX, and CAT activities. Furthermore, the combined protocol further decreased the liver morphological score compared with solo treatment. Discussion and conclusion: Overall, the results indicate that the H. scoparia flavonoid-enriched fraction could be a promising candidate for future application as a pharmacological preconditioning agent against hepatic IRI.

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Sequential changes of connexin32 and connexin26 in ischemia-reperfusion of the liver in rats

Cited by 10 publications

References 29 publications

Gap junctions and non-neoplastic liver disease

Gap junctions and non-neoplastic liver disease

Gap junctions in liver disease: Implications for pathogenesis and therapy

Protective effects ofHammada scopariaflavonoid-enriched fraction on liver injury induced by warm ischemia/reperfusion

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