Effects of Nuclear Factor-κB Inhibitors on Colon Anastomotic Healing in Rats

Bedirli, Abdülkadir; Salman, Bülent; Paşaoğlu, Hatîce; Ofluoglu, Ebru; Şakrak, Ömer

doi:10.1016/j.jss.2010.01.028

Cited by 17 publications

(11 citation statements)

References 24 publications

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“…As we all known, production of cytokines and chemokines by immune/inflammatory cells that activate transcription factors such as NF-κB in pre-malignant cells to induce genes that stimulate cell proliferation,survival, and growth, as well as angiogenesis, and invasiveness motility [32]–[35]. In details, NF-κB (p65) is located in cytoplasm and bounds to IκB as an inactive complex [32], [33].…”

Section: Discussionmentioning

confidence: 99%

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Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation

Zhong

Wang

et al. 2014

PLoS ONE

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Phytogenic compounds with anti-oxidant and anti-inflammatory properties, such as ginsenoside metabolite compound K (CK) or berberine (BBR), are currently discussed as promising complementary agents in the prevention and treatment of cancer and inflammation. The latest study showed that ginsenoside Rb1 and its metabolites could inhibit TNBS-induced colitis injury. However, the functional mechanisms of anti-inflammation effects of ginsenoside, particularly its metabolite CK are still not clear. Here, using dextran sulfate sodium (DSS)-induced colitis in mice, clinical parameters, intestinal integrity, pro-inflammatory cytokines production, and signaling pathways in colonic tissues were determined. In mild and sever colitis mice, CK and BBR (as a positive agent) alleviated colitis histopathology injury, ameliorated myeloperoxidase (MPO) activity, reduced pro-inflammatory cytokines production, such as, IL-6, IL-1β, TNF-α, and increased anti-inflammatory cytokine IL-10 production in both mice colon tissues and blood. Nevertheless, the results revealed that CK and BBR inhibited NF-κB p65 nuclear translocation, downregulated p-IκBα and upregulated IκBα, indicating that CK, as well as BBR, suppressed the activation of the NF-κB pathway in the progression of colitis with immunofluorescence, immunohistochemical and western blotting analysis. Furthermore, CK inhibited pro-inflammatory cytokines production in LPS-activated macrophages via down-regulation of NF-κB signaling pathway. Taken together, our results not only reveal that CK promotes the recovery of the progression of colitis and inhibits the inflammatory responses by suppressing NF-κB activation, but also suggest that CK downregulates intestinal inflammation through regulating the activation of macrophages and pro-inflammatory cytokines production.

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Section: Discussionmentioning

confidence: 99%

“…In details, NF-κB (p65) is located in cytoplasm and bounds to IκB as an inactive complex [32], [33]. The phosphorylation and subsequent degradation of IκB result in separation of the complex, and then NF-κB is activated.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation

Zhong

Wang

et al. 2014

PLoS ONE

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“…Accordingly, targeting capacity of several pharmacological agents has led to inhibition of MMP-9; these agents include numerous nutraceutical molecules. Among these, sulforaphane, 8 , 32 epigallocatechingallate, 14 , 33 , 34 curcumin, 35 , 36 resveratrol, 37 , 38 proanthocyanidins 39 and lycopene 40 have all been proved to inhibit MMP-9 expression/ secretion. More interestingly, all of the above-mentioned diet-derived molecules also abrogated the NF-κB signaling pathway which regulates MMP-9 expression.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological targeting of β-adrenergic receptor functions abrogates NF-κB signaling and MMP-9 secretion in medulloblastoma cells

Annabi¹,

Vaillancourt-Jean²,

Weil³

et al. 2010

OTT

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Targeting of the vascular endothelium compartment explains, in part, the therapeutic efficacy of the nonselective β-adrenergic antagonist propranolol against common endothelial tumors such as hemangiomas. In vitro, the antiangiogenic biological activity of propranolol was shown to inhibit human brain microvascular endothelial cell tubulogenesis. However, possible interference of propranolol with cell signaling associated with the tumoral compartment remains unexplored. We therefore assessed the potency of propranolol against a pediatric brain tumor- derived DAOY medulloblastoma cell model. Gene expression of β1-, β2-, and β3-adrenergic receptors was confirmed in DAOY cells by semiquantitative RT-PCR. We next found that propranolol dose-dependently inhibited induction of the key extracellular matrix-degrading and blood–brain barrier disrupting enzyme matrix metalloproteinase- 9 (MMP-9) by phorbol 12-myristate 13-acetate (PMA). Propranolol not only inhibited PMA- induced phosphorylation of the extracellular signal-regulated kinase (Erk), but also that of IkappaB (IκB), preventing the IκB phosphorylation which is a prerequisite for IκB degradation. Propranolol inhibition of IκB phosphorylation was shown to occur with optimal efficacy at 30 μM. Although propranolol, at up to 100 μM, did not affect cell viability, it potentiated PMA- mediated signaling that ultimately led to diminished phosphorylation of Akt. The anti-Erk and anti-Akt phosphorylation effects are both suggestive of antiproliferative and antisurvival signaling, respectively. Our data are therefore indicative of a pharmacological role for propranolol against β-adrenergic receptor signaling functions involving the nuclear factor-kappaB-mediated regulation of MMP-9.

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“…RSV (>99% pure, from Sigma, Stockholm, Sweden) was administrated orally by orogastric tube at a concentration of 0.5 mg/kg/day for 7 days. In the literature, the reported dose of resveratrol to be administered varies from 0.5 to 20 oral mg/kg per day in animal models 16,17 .…”

Section: Animalsmentioning

confidence: 99%

The Protective Effect of Resveratrol in Experimentally Induced Non-Sterile Clean Wound Inflammation in Rats

Hişmioğulları¹,

Hişmioğulları²,

Yavuz³

et al. 2013

Kafkas Univ Vet Fak Derg

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The effects of resveratrol on haematological and biochemical parameters were investigated in rats that had inflammation induced by experimental non-sterile clean wound technique. Twenty four male Wistar-Albino rats weighing 250-300 g were placed into three groups of eight after matching for age, sex and weight. In the sham-operated and resveratrol-treated groups, a 4-cm incision was made on the median line of the rats in order to create a wound. Resveratrol group was administrated resveratrol daily at a dose of 0.5 mg/kg/day for seven days. At the end of seven days, blood samples were obtained prior to sacrification and then analysed for hematological and biochemical parameters. The mean concentration of the inflammatory markers as CRP, WBC and LDH were significantly lower in resveratrol-treated group compared to the shame-operated group (P<0.05). Similarly, the mean values for WBC and LDH activity were significantly decreased in resveratrol-treated group compared to the control group (P<0.05). Resveratrol-treated group had significantly lower triglyceride concentration whereas sham-operated group had significantly higher glucose concentration when compared with the control values (P<0.001 and P<0.05, respectively). The results of the present study indicate that resveratrol attenuates inflammation and restores the alterations in blood chemistry induced by experimental clean wound inflammation in rats. Keywords: Resveratrol, Inflammation, Biochemical parameters, Haematological parameters, Wound Sıçanlarda Deneysel Oluşturulan Steril Olmayan Temiz Yara İnflamasyonunda Resveratrolün Koruyucu Etkisi ÖzetDeneysel steril olmayan temiz yara tekniği ile indüklenmiş inflamasyona sahip sıçanlarda, resveratrolün hematolojik ve biyokimyasal parametrelere olan etkisi araştırıldı. Yirmidört adet, 250-300 g ağırlığında Wistar-Albino sıçanları; yaş, cinsiyet ve ağırlıkları eşleşecek şekilde, 3 gruba yerleştirildi. Sham-operasyonu geçirmiş ve resveratrol almış gruplarda, sıçanların median hattı boyunca 4 cm'lik bir ensizyon yapılarak yara oluşturuldu. Resveratrol, 7 gün boyunca, 0.5 mg/kg/gün dozunda verildi. Yedi günün sonunda, hayvanlar öldürülmeden önce kan numuneleri alındı ve hematolojik ile biyokimyasal parametreler yönünden analiz edildi. Resveratrol almış grupta; CRP, WBC ve LDH gibi yangı belirteçleri, sham-operasyonu geçirmiş grup ile karşılaştırıldığında belirgin olarak düşüktü (P<0.05). Benzer şekilde, resveratrol almış grubun, WBC ve LDH aktivitelerinin ortalama değerleri, kontrol grubu ile karşılaştırıldığında, belirgin olarak düşüktü (P<0.05). Kontrol değerleriyle karşılaştırıldığında, resveratrol almış grup, belirgin olarak daha düşük trigliserid konsantrasyonuna sahipken, sham-operasyonu geçirmiş grup da belirgin olarak daha yüksek glukoz konsantrasyonuna sahipti (sırasıyla, P<0.001 ve P<0.05). Bu çalışmanın sonuçları, resveratrolün sıçanlarda inflamasyonu zayıflattığını ve kan kimyasında deneysel temiz yara inflamasyonu ile indüklenme sonucu oluşan değişiklikleri onardığını göstermektedir.

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Effects of Nuclear Factor-κB Inhibitors on Colon Anastomotic Healing in Rats

Cited by 17 publications

References 24 publications

Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation

Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation

Pharmacological targeting of β-adrenergic receptor functions abrogates NF-κB signaling and MMP-9 secretion in medulloblastoma cells

The Protective Effect of Resveratrol in Experimentally Induced Non-Sterile Clean Wound Inflammation in Rats

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Effects of Nuclear Factor-κB Inhibitors on Colon Anastomotic Healing in Rats

Cited by 17 publications

References 24 publications

Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation

Ginsenoside Metabolite Compound K Promotes Recovery of Dextran Sulfate Sodium-Induced Colitis and Inhibits Inflammatory Responses by Suppressing NF-κB Activation

Pharmacological targeting of &beta;-adrenergic receptor functions abrogates NF-&kappa;B signaling and MMP-9 secretion in medulloblastoma cells

The Protective Effect of Resveratrol in Experimentally Induced Non-Sterile Clean Wound Inflammation in Rats

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Pharmacological targeting of β-adrenergic receptor functions abrogates NF-κB signaling and MMP-9 secretion in medulloblastoma cells