Malondialdehyde in early phase of acute pancreatitis

Hernández, Vicent; Miranda, María; Pascual, Isabel; Sánchiz, Vicente; Almela, Pedro; Añón, R; Cuadrado, Esperanza; Sanz, María I.; Mínguez, Miguel; Mora, Francisco; Romero, Francisco J.; Benages, A

doi:10.4321/s1130-01082011001100002

Cited by 12 publications

(11 citation statements)

References 33 publications

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“…Malondialdehyde (MDA) is the principal and most studied product of polyunsaturated fatty acid peroxidation. So far, oxidative stress have been assessed by measuring the level of antioxidants or the concentration of substances derived from the action of oxygen free radicals on biological molecules, and measurement of MDA is considered an effective marker of oxidative stress in a biological sample [38]. In our study, it could be showed that corilagin has a significant effect on MDA expression, which implies corilagin has a strong potential to suppress oxidative stress when cholestasis occurs.…”

Section: Discussionmentioning

confidence: 69%

Anti-inflammatory and anti-oxidative effects of corilagin in a rat model of acute cholestasis

Jin

Cheng

Tao³

et al. 2013

BMC Gastroenterol

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BackgroundNowadays, treatments for cholestasis remain largely nonspecific and often ineffective. Recent studies showed that inflammatory injuries and oxidative stress occur in the liver with cholestasis. In this study, we would use corilagin to treat the animal model of acute cholestasis in order to define the activity to interfere with inflammation-related and oxidative stress pathway in cholestatic pathogenesis.MethodsRats were administrated with alpha-naphthylisothiocyanate to establish model of cholestasis and divided into corilagin, ursodeoxycholic acid, dexamethasone, model and normal groups with treatment of related agent. At 24h, 48h and 72h time points after administration, living condition, serum markers of liver damage, pathological changes of hepatic tissue, nuclear factor (NF)-kappaB, myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were examined and observed.ResultsCompared to model group, corilagin had remarkable effect on living condition, pathological manifestation of liver tissue, total bilirubin, direct bilirubin, (P<0.01), but no effect on alanine aminotransferase (ALT) and aspartate aminotransferase (AST). With corilagin intervention, levels of MPO, MDA and translocation of NF-κB were notably decreased, and levels of SOD and NO were markedly increased (P<0.05 or P<0.01).ConclusionsIt is shown that corilagin is a potential component to relieve cholestasis through inflammation-related and oxidation-related pathway.

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Section: Discussionmentioning

confidence: 69%

Anti-inflammatory and anti-oxidative effects of corilagin in a rat model of acute cholestasis

Jin

Cheng

Tao³

et al. 2013

BMC Gastroenterol

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“…Moreover, clinical studies have also verified the presence of oxidative stress during AP [97] . Indeed, lipid peroxidation, myeloperoxidase activity, and protein carbonyls increase in plasma of patients with SAP [98–100] . All these parameters are generally related to severity of the disease both in clinical and experimental studies.…”

Section: Oxidative Stress In Acute Pancreatitismentioning

confidence: 96%

“…All these parameters are generally related to severity of the disease both in clinical and experimental studies. Thus, the increase in malondialdehyde (MDA) levels correlates with tissue injury in AP [100,101] . Furthermore, superoxide radical and lipid peroxide levels also increase in blood of patients and animals with AP, and these changes correlate with the degree of AP severity [85,102] .…”

Section: Oxidative Stress In Acute Pancreatitismentioning

confidence: 99%

Redox signaling in acute pancreatitis

et al. 2015

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Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On the other hand, the release of extracellular hemoglobin into the circulation from the ascitic fluid in severe necrotizing pancreatitis enhances lipid peroxidation in plasma and the inflammatory infiltrate into the lung and up-regulates the HIF–VEGF pathway, contributing to the systemic inflammatory response. Therefore, redox signaling and oxidative stress contribute to the local and systemic inflammatory response during acute pancreatitis.

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“…Hence many authors posit the presence of a window period where all measures intended to control and modulate inflammation may improve the final result as inferred from this interesting paper by Hernández et al (16), even though the attribution of an initial tissue damage mechanism to free oxygen radicals is difficult to establish given that patients usually delay their seeking help and are seen when these pathogenic mechanisms for acinar cell damage are already ongoing. Besides their pathophysiological involvement at process onset, they may also be generated and contribute to progression.…”

mentioning

confidence: 99%

“…Thus, different investigators have analyzed MDA levels in the early stages of both serious and mild acute pancreatitis with conflicting results (10)(11)(12)(13)(14)(15). The measurement process is key to differentiate true MDA levels from those of other thiobarbituric acid reactive substances, as pointed out by Hernández et al (16) in their paper published in this issue of the Spanish Journal of Gastroenterology. Researchers use a high-resolution liquid chromatography system to measure free serum MDA levels.…”

mentioning

confidence: 99%

Oxidative stress and acute pancreatitis

Martín

Carrillo-Alcaraz

2011

Rev. esp. enferm. dig.

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Acute pancreatitis (AP) is a pancreatic inflammatory condition characterized by abdominal pain and increased pancreatic enzyme levels in the blood and urine, with its diagnosis relying on these two premises. Regardless of its trigger, once active the process enters the common pathway of the local and systemic inflammatory response, and severity depends on response intensity (1).The relevance of AP depends not only on potential complicated outcomes but also its high frequency -in our country an incidence of 15,000 new cases yearly was estimated, but it should be highlighted that 3.5-19% of cases experience no pain, and 13-42% are only diagnosed in necropsy studies (2). Clinical course is usually benign, and clinical signs and symptoms, as well as amylasemia/amylasuria levels, decrease within a few days; however, around 20% of cases develop complications both at the local and systemic levels, with pancreatic necrosis being most common and relevant (a good correlation exists between necrosis extent and patient outcome). AP-related mortality still affects around 10% of patients; half of deaths occur during the first two weeks, usually related to distributive shock and multiple organ failure syndrome; the rest occur later in the course of the disease and result from complications related to the development of pancreatic necrosis and its complications.The pathophysiology of AP is complex and involves several inflammatory pathways. The initial trigger is the activation within the pancreatic parenchyma of various proteolytic enzymes, usually promoted by the presence of bile and duodenal contents inside pancreatic ducts. Severe forms also exhibit a disbalance in the protease-antiprotease system, which activates the complement system with release of factor C5a, which in turn stimulates macrophage and neutrophil recruitment; this further promotes intraperitoneal inflammation and cytokine activation via transcription factors such as nuclear factor kappa B (NFκB). The release of activated cytokines involves both proinflammatory (tumor necrosis factor, interleukins IL-1, IL-6 and IL-8, and platelet-activating factor) and antiinflammatory (interleukins IL-2, IL-10 and IL-11) cytokines. Other mediators involved include arachidonic acid metabolites (prostaglandins, plateletactivating factor, and leukotrienes), nitric oxide, various proteolytic and lipolytic enzymes, and reactive oxygen metabolites, which overcome the clearing capacity of endogenous antioxidant systems. The most powerful oxygen metabolite released by leukocytes is ClOH, whereas polymorphonuclear elastase is the most destructive enzyme released (3,4). Finally, acinar damage induces the expression of endothelial adhesion molecules such as VCAM-1 (vascular cell adhesion molecule), which further amplifies the inflammatory response (5) and results in a vicious circle that determines a widespread involvement of the vascular endothelium, which in turn results in vasodilation, increased capillary permeability and interstitial edema. In fact, in most serious cases the inf...

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Malondialdehyde in early phase of acute pancreatitis

Cited by 12 publications

References 33 publications

Anti-inflammatory and anti-oxidative effects of corilagin in a rat model of acute cholestasis

Anti-inflammatory and anti-oxidative effects of corilagin in a rat model of acute cholestasis

Redox signaling in acute pancreatitis

Oxidative stress and acute pancreatitis

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