Therapeutic effects of ellagic acid on L-arginin ınduced acute pancreatitis

Yılmaz, Edip Erdal; Bozdağ, Zübeyir; İbiloğlu, İbrahim; Arıkanoğlu, Zülfü; Yazgan, Ümit Can; Kaplan, İbrahim; Gümüş, Metehan; Atamanalp, Sabri Selçuk

doi:10.1590/s0102-865020160060000006

Cited by 26 publications

(19 citation statements)

References 25 publications

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“…This is compatible with the LPS induced increase in serum IL-6 level in the present study which is also in agreement with Liu and Cheng (2016) and Weifeng et al (2016). Yılmaz et al (2016) demonstrated that cytokines caused acute lung damage by affecting phospholipids, surfactant and increased vessel permeability. Therefore, LPS induced ALI is most probably related to an increase of both cytokines and nitrosative stress levels (Zhang et al 2016).…”

Section: Immunohistochemical Assessment Of Inossupporting

confidence: 93%

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats

Ali¹,

Abdel-Hamid²,

Toni³

2018

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. Hydrogen sulfide (H2S) is gasotransmitter which plays an important role in human physiology. In this study, we aimed to check the effect of H2S treatment on acute lung inflammation (ALI). Thirty-six adult male albino rats were used and divided into: control group, ALI group which was intraperitoneally (i.p.) injected with lipopolysaccharide (LPS) at a dose of 5 mg/kg body weight, ALI group treated by the H2S donor; sodium hydrosulfide (NaHS) at a dose of 10 mg/kg body weight i.p. and ALI group treated by i.p. injection of 80 mg/kg body weight DL- propargylglycine (PAG) which is an inhibitor of endogenous H2S synthesis. Serum was obtained to determine interleukin-6 (IL-6) levels. Lipid peroxides and total antioxidant capacity (TAC) levels were measured in lung. Lung histopathology and expression of inducible nitric oxide synthase (iNOS) were also done. Results showed that NaHS improved lung inflammation through its inhibitory effect on iNOS expression, decreasing the levels of IL-6 and lipid peroxides and increasing TAC levels. But, ALI was exacerbated with PAG administration. In conclusion, the results proved that H2S has a protective effect against LPS induced ALI due to its anti-nitrative, anti-oxidant and anti-inflammatory properties.

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Section: Immunohistochemical Assessment Of Inossupporting

confidence: 93%

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats

Ali¹,

Abdel-Hamid²,

Toni³

2018

gpb

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“…The results of the present study demonstrated that administration of L-arginine to rats produced severe AP, which was confirmed with histopathological examination. In addition, marked increase in the serum levels of pancreatic enzymes, NO, CORT and TNF-α, and pancreatic MDA and iNOS levels were detected what is in a line with previous studies (Ucmak et al 2016;Yilmaz et al 2016;Aziz et al 2017).…”

Section: Discussionsupporting

confidence: 91%

“…i.p. with an interval of 1 h, the rats were sacrificed by decapitation 24 h after last L-arginine administration (Yilmaz et al 2016); NaHS+AP group -each rat was i.p. injected with NaHS at a dose of 10 mg/kg b.w., which was given 1 h before induction of AP (Rao et al 2015), the rats were sacrificed by decapitation 24 h later; Leptin+AP group -each rat was i.p.…”

Section: Methodsmentioning

confidence: 99%

Comparing the preventive effect of sodium hydrosulfide, leptin, and curcumin against L-arginine induced acute pancreatitis in rats: role of corticosterone and inducible nitric oxide synthase

Ragy

Ali

Toni

2019

Endocrine Regulations

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Objectives. Acute pancreatitis (AP) is a life-threatening condition. Using antioxidants in AP is insufficient and conflicting. Therefore, this study compared the effect of hydrogen sulfide (H2S) donor, sodium hydrosulfide (NaHS), leptin or curcumin pretreatment on AP induced by L-arginine.Methods. Forty adult male rats were used and classified into: 1) control; 2) AP group [each rat was intraperitoneally (i.p.) injected with 2 doses of L-arginine of 250 mg/100 g body weight (b.w.) with an interval of 1 h]; 3) NaHS+AP group (each rat was i.p. injected with 10 mg/kg b.w. of NaHS 1 h before induction of AP); 4) leptin+AP group (each rat was pretreated with 10 μg/kg b.w. of leptin 30 min before induction of AP; and 5) curcumin+AP group (in which rats were i.p. injected with 150 mg/kg b.w. of curcumin 30 min before induction of AP). Serum amylase, lipase, nitric oxide (NO), tumor necrosis factor alpha (TNF-α), and corticosterone (CORT) levels were assayed. In addition, pancreatic tissues were obtained for histopathological examination and malondialde-hyde (MDA), total antioxidant capacity (TAC), and inducible nitric oxide synthase (iNOS) levels were measured.Results. All AP treated groups showed significant decrease in serum levels of pancreatic enzymes, NO, and TNF-α, and pancreatic MDA and iNOS levels, while TAC levels were significantly increased. NaHS caused more limitation of inflammation than leptin and curcumin by affecting iNOS. Leptin was more potent than curcumin due to the stimulatory effect of leptin on glucocorticoid release to counteract inflammation.Conclusions. NaHS was more effective in AP amelioration than the leptin and curcumin.

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“…Apart from its well-known antioxidative effects, ellagic acid has also been shown to exert potent anti-inflammatory activities [88]. For this reason, several studies have emphasized the potential of ellagic acid as a candidate for the treatment of many chronic inflammatory diseases and conditions [91][92][93]. In this review, we will cite the most relevant studies, specifically those focused on the mechanism of action.…”

Section: Anti-inflammatory Activity Of Ellagic Acidmentioning

confidence: 99%

A Pharmacological Update of Ellagic Acid

et al. 2018

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Ellagic acid is a common metabolite present in many medicinal plants and vegetables. It is present either in free form or as part of more complex molecules (ellagitannins), which can be metabolized to liberate ellagic acid and several of its metabolites, including urolithins. While ellagic acidʼs antioxidant properties are doubtless responsible for many of its pharmacological activities, other mechanisms have also been implicated in its various effects, including its ability to reduce the lipidemic profile and lipid metabolism, alter pro-inflammatory mediators (tumor necrosis factor-α, interleukin-1β, interleukin-6), and decrease the activity of nuclear factor-κB while increasing nuclear factor erythroid 2-related factor 2 expression. These events play an important role in ellagic acidʼs anti-atherogenic, anti-inflammatory, and neuroprotective effects. Several of these activities, together with the effect of ellagic acid on insulin, glycogen, phosphatases, aldose reductase, sorbitol accumulation, advanced glycation end-product formation, and resistin secretion, may explain its effects on metabolic syndrome and diabetes. In addition, results from recent research have increased the interest in ellagic acid, both as a potential protective agent of the liver and skin and as a potential anticancer agent, due to the specific mechanisms affecting cell proliferation, apoptosis, DNA damage, and angiogenesis and its aforementioned anti-inflammatory properties. Taken together, these effects make ellagic acid a highly interesting compound that may contribute to different aspects of health; however, more studies are needed, especially on the compoundʼs pharmacokinetic profile. In this review, we selected papers published from 2005 to the present.

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Therapeutic effects of ellagic acid on L-arginin ınduced acute pancreatitis

Cited by 26 publications

References 25 publications

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats

H2S attenuates acute lung inflammation induced by administration of lipopolysaccharide in adult male rats

Comparing the preventive effect of sodium hydrosulfide, leptin, and curcumin against L-arginine induced acute pancreatitis in rats: role of corticosterone and inducible nitric oxide synthase

A Pharmacological Update of Ellagic Acid

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