Amentoflavone inhibits iNOS, COX-2 expression and modulates cytokine profile, NF-κB signal transduction pathways in rats with ulcerative colitis

Sakthivel, Kunnathur Murugesan; Guruvayoorappan, Chandrasekharan

doi:10.1016/j.intimp.2013.09.022

Cited by 102 publications

(60 citation statements)

References 32 publications

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“…As shown in Figure 2, the mRNA levels of TLR1, 2,3,4,6,7,8, and 9 in the CBLB502 treatment group were significantly lower than in the model group (P<0.05). The results of RT-PCR demonstrated that CBLB502 can reduce the TLR expression in the mouse colon.…”

Section: Cblb502 Reduces the Tlrs Expression In Micementioning

confidence: 87%

“…In model group animals, the concentration of TNF-α in serum was 140.11±12.70 ng/mL, which was lower than protein levels in the control group (173.86±29.26 ng/mL, P<0.05). The mRNA levels of TLR1,2,3,4,6,7,8, and 9 in the CBLB502 treatment group were significantly lower than in the model group (P<0.05). Western blot revealed that CBLB502 also reduced NF-κB expression in the mouse colon, but that NF-κB expression was not significantly lower than the model group.…”

mentioning

confidence: 79%

“…Western blot revealed that CBLB502 also reduced NF-κB expression in the mouse colon but that NF-κB expression was not significantly lower than the model group (P>0.05), as shown in 2,3,4,6,7,8, and 9 in the CBLB502 treatment group were significantly lower than those in the model group. *, P<0.05; **, P<0.01.…”

Section: Cblb502 Reduces the Expression Of Nf-κb In Micementioning

confidence: 91%

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CBLB502 administration protects gut mucosal tissue in ulcerative colitis by inhibiting inflammation

Xu¹,

Dong

et al. 2016

Ann. Transl. Med.

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Background: Ulcerative colitis (UC) is a nonspecific inflammatory disease for which medications and therapeutic strategies have only been moderately successful. CBLB502, a toll-like receptor 5 (TLR5) agonist derived from Salmonella flagellin, exhibits anticancer and radioprotective activities via modulation of TLRs and the nuclear factor kappa B (NF-κB) signaling pathway and can protect against acute renal ischemic failure. In this study, we intend to examine the effects of CBLB502 on both TLR responses and the interleukin (IL) and NF-κB signaling pathways in UC treatment.Methods: The UC mouse model was prepared in BALB/c mice by administering 2,4,6-trinitrobenzene sulfonic acid (TNBS). CBLB502 was used as the therapeutic drug. After CBLB502 therapy, the IL and tumor necrosis factor-α (TNF-α) levels were measured by ELISA. Total RNA and protein of colon samples was extracted.Results: We found that CBLB502 had a distinctive therapeutic effect in the UC model. In control group animals, IL-10 expression in serum was 91.48±24.38 ng/mL; this was higher than in the model group (59.36±14.46 ng/mL, P<0.05) or the treatment group (54.29±5.83 ng/mL, P<0.05). In model group animals, the concentration of TNF-α in serum was 140.11±12.70 ng/mL, which was lower than protein levels in the control group (173.86±29.26 ng/mL, P<0.05). The mRNA levels of TLR1,2,3,4,6,7,8, and 9 in the CBLB502 treatment group were significantly lower than in the model group (P<0.05). Western blot revealed that CBLB502 also reduced NF-κB expression in the mouse colon, but that NF-κB expression was not significantly lower than the model group.Conclusions: CBLB502 can reduce mucosal damage induced by TNBS and inhibit inflammation and TLR expression. The inhibition of UC by CBLB502 is strictly TLR-IL-dependent and is dose-dependent within the efficacious dose range. Therefore, our results suggested that CBLB502 might be a candidate drug for the treatment of UC.

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Section: Cblb502 Reduces the Tlrs Expression In Micementioning

confidence: 87%

mentioning

confidence: 79%

Section: Cblb502 Reduces the Expression Of Nf-κb In Micementioning

confidence: 91%

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CBLB502 administration protects gut mucosal tissue in ulcerative colitis by inhibiting inflammation

Xu¹,

Dong

et al. 2016

Ann. Transl. Med.

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“…Therefore, we measured the levels of key antioxidant enzymes, catalase, GPx1, and SOD1, which are shown to be reduced in models of IBD (Cetinkaya et al, 2006;Sakthivel and Guruvayoorappan, 2013;Ren et al, 2014). Figure 5A shows that the level of each enzyme increases maximally when Clamidine is dosed at 5 mg/ml (12 mM) in ANA-1 murine macrophages.…”

Section: Resultsmentioning

confidence: 99%

Inhibiting Protein Arginine Deiminases Has Antioxidant Consequences

Witalison

Cui

Hofseth

et al. 2015

J Pharmacol Exp Ther

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Ulcerative colitis is a dynamic, idiopathic, chronic inflammatory condition that carries a high colon cancer risk. We previously showed that Cl-amidine, a small-molecule inhibitor of the protein arginine deiminases, suppresses colitis in mice. Because colitis is defined as inflammation of the colon associated with infiltration of white blood cells that release free radicals and citrullination is an inflammationdependent process, we asked whether Cl-amidine has antioxidant properties. Here we show that colitis induced with azoxymethane via intraperitoneal injection 1 2% dextran sulfate sodium in the drinking water is suppressed by Cl-amidine (also given in the drinking water).Inducible nitric oxide synthase, an inflammatory marker, was also downregulated in macrophages by Cl-amidine. Because epithelial cell DNA damage associated with colitis is at least in part a result of an oxidative burst from overactive leukocytes, we tested the hypothesis that Cl-amidine can inhibit leukocyte activation, as well as subsequent target epithelial cell DNA damage in vitro and in vivo. Results are consistent with this hypothesis, and because DNA damage is a procancerous mechanism, our data predict that Clamidine will not only suppress colitis, but we hypothesize that it may prevent colon cancer associated with colitis.

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“…Amentoflavone의 기본적인 화학구조는 (Sakthivel & Guruvayoorappan, 2013; 가지고 있다 (Barbouti et al, 2002 (Liotta et al, 1980;Bonfil et al, 1989;Liotta & Stetler, 1990;Matrisian, 1990 (Glimcher, 1989;Bailly et al, 1990 Results and Discussion Figure 3C). Figure 4B).…”

mentioning

confidence: 90%

Effects of Amentoflavone on Anti-inflammation and Cytoprotection

Lee¹,

Han²,

An³

et al. 2016

Asian J Beauty Cosmetol

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Purpose: This study aimed to investigate the potential of amentoflavone as an antiaging material for cosmetics through examining antioxidant and antiwrinkle effects. Methods: To check the antioxidant and antiwrinkle effects of amentoflavone, we performed various experiments such as in vitro antioxidant assays, quantitative real-time PCR, SA-β-galactosidase assay, and DCF-DA assay. Results: We confirmed that the cell viability of amentoflavone is increased in cytotoxic condition. Amentoflavone also had an antioxidant effect like BHT. The expression in mRNA level of antioxidant enzymes such as SOD1 and CAT was increased in a dosedependent manner. In case of wrinkle, the expression in mRNA level of MMP1 and MMP3 was decreased but the expression of COL1A1 was dose-dependently increased. Also, amentoflavone markedly reduced the expression of SA-β-galactosidase. Conclusion: As mentioned above, we found that amentoflavone had effects on preventing skin aging and thought that amentoflavone can be a valulable material for antiaging cosmetics.

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Amentoflavone inhibits iNOS, COX-2 expression and modulates cytokine profile, NF-κB signal transduction pathways in rats with ulcerative colitis

Cited by 102 publications

References 32 publications

CBLB502 administration protects gut mucosal tissue in ulcerative colitis by inhibiting inflammation

CBLB502 administration protects gut mucosal tissue in ulcerative colitis by inhibiting inflammation

Inhibiting Protein Arginine Deiminases Has Antioxidant Consequences

Effects of Amentoflavone on Anti-inflammation and Cytoprotection

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