The Comparison of the Effects of Ellagic Acid and Diclofenac Sodium on Intra-Abdominal Adhesion: An In Vivo Study in the Rat Model

Allahverdi, Tülay Diken; Allahverdi, Ertuğrul; Yayla, Sadık; Deprem, Turgay; Merhan, Oğuz; Vural, Sevil Atalay

doi:10.9738/intsurg-d-14-00065.1

Cited by 12 publications

(8 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, NF-κB was a potential target for the anti-inflammatory effect of ellagic acid incorporated into the normal diet (0.5 %) of mice in an ulcerative colitis experimental model [97]. Similar results for ellagic acid as an anti-inflammatory agent through modulation of the NF-κB activation pathway have been observed in several other studies [98][99][100][101][102].…”

Section: Anti-inflammatory Activity Of Ellagic Acidsupporting

confidence: 76%

A Pharmacological Update of Ellagic Acid

et al. 2018

View full text Add to dashboard Cite

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.

show abstract

Section: Anti-inflammatory Activity Of Ellagic Acidsupporting

confidence: 76%

A Pharmacological Update of Ellagic Acid

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Blocking thrombin-activated fibrinolysis inhibitor reduces adhesions (167). Dexmedetomidine, a selective a 2 -adrenergic with secondary antioxidant and antiinflammatory effects (168), bromelain, a pineapple extract with fibrinolytic and antiinflammatory properties (169), clinoquinol, which limits inflammation and fibroblastic activity (170), vitamin C and vitamin E (171), ellagic acid, with antioxidant and antiinflammatory properties (172), and biodegradable micelles (173) all reduce adhesion formation.…”

Section: Discussionmentioning

confidence: 99%

Role of the peritoneal cavity in the prevention of postoperative adhesions, pain, and fatigue

Koninckx¹,

Gomel

Ussia³

et al. 2016

Fertility and Sterility

109

View full text Add to dashboard Cite

A surgical trauma results within minutes in exudation, platelets, and fibrin deposition. Within hours, the denuded area is covered by tissue repair cells/macrophages, starting a cascade of events. Epithelial repair starts on day 1 and is terminated by day 3. If repair is delayed by decreased fibrinolysis, local inflammation, or factors in peritoneal fluid, fibroblast growth starting on day 3 and angiogenesis starting on day 5 results in adhesion formation. For adhesion formation, quantitatively more important are factors released into the peritoneal fluid after retraction of the fragile mesothelial cells and acute inflammation of the entire peritoneal cavity. This is caused by mechanical trauma, hypoxia (e.g., CO pneumoperitoneum), reactive oxygen species (ROS; e.g., open surgery), desiccation, or presence of blood, and this is more severe at higher temperatures. The inflammation at trauma sites is delayed by necrotic tissue, resorbable sutures, vascularization damage, and oxidative stress. Prevention of adhesion formation therefore consists of the prevention of acute inflammation in the peritoneal cavity by means of gentle tissue handling, the addition of more than 5% NO to the CO pneumoperitoneum, cooling the abdomen to 30°C, prevention of desiccation, a short duration of surgery, and, at the end of surgery, meticulous hemostasis, thorough lavage, application of a barrier to injury sites, and administration of dexamethasone. With this combined therapy, nearly adhesion-free surgery can be performed today. Conditioning alone results in some 85% adhesion prevention, barriers alone in 40%-50%.

show abstract

“…Surgeons have been trying to minimize adhesions through meticulous surgical techniques, minimizing blood loss, shortening surgical time and preoperative heparin, administering anti-inflammatory steroids and antioxidant substances, and using mechanical adhesion barriers [6,44,[71][72][73][74][75][76]. Our observations that adhesions were proportionally higher in cases with blood loss >500 mL, operative time >200 min, or >7 uterine incisions reiterate the importance of these factors in reducing fibrosis.…”

Section: Adhesionsmentioning

confidence: 69%

Intraperitoneal Triamcinolone Reduces Postoperative Adhesions, Possibly through Alteration of Mitochondrial Function

Purandare

Kramer

Minchella

et al. 2022

JCM

View full text Add to dashboard Cite

Adhesions frequently occur postoperatively, causing morbidity. In this noninterventional observational cohort study, we enrolled patients who presented for repeat abdominal surgery, after a history of previous abdominal myomectomy, from March 1998 to June 20210 at St. Vincent’s Catholic Medical Centers. The primary outcome of this pilot study was to compare adhesion rates, extent, and severity in patients who were treated with intraperitoneal triamcinolone acetonide during the initial abdominal myomectomy (n = 31) with those who did not receive any antiadhesion interventions (n = 21), as documented on retrospective chart review. Adhesions were blindly scored using a standard scoring system. About 32% of patients were found to have adhesions in the triamcinolone group compared to 71% in the untreated group (p < 0.01). Compared to controls, adhesions were significantly less in number (0.71 vs. 2.09, p < 0.005), severity (0.54 vs. 1.38, p < 0.004), and extent (0.45 vs. 1.28, p < 0.003). To understand the molecular mechanisms, human fibroblasts were incubated in hypoxic conditions and treated with triamcinolone or vehicle. In vitro studies showed that triamcinolone directly prevents the surge of reactive oxygen species triggered by 2% hypoxia and prevents the increase in TGF-β1 that leads to the irreversible conversion of fibroblasts to an adhesion phenotype. Triamcinolone prevents the increase in reactive oxygen species through alterations in mitochondrial function that are HIF-1α-independent. Controlling mitochondrial function may thus allow for adhesion-free surgery and reduced postoperative complications.

show abstract

The Comparison of the Effects of Ellagic Acid and Diclofenac Sodium on Intra-Abdominal Adhesion: An In Vivo Study in the Rat Model

Cited by 12 publications

References 26 publications

A Pharmacological Update of Ellagic Acid

A Pharmacological Update of Ellagic Acid

Role of the peritoneal cavity in the prevention of postoperative adhesions, pain, and fatigue

Intraperitoneal Triamcinolone Reduces Postoperative Adhesions, Possibly through Alteration of Mitochondrial Function

Contact Info

Product

Resources

About