Carvedilol attenuates paraquat-induced lung injury by inhibition of proinflammatory cytokines, chemokine MCP-1, NF-κB activation and oxidative stress mediators

Amirshahrokhi, Keyvan; Khalili, Ali-Reza

doi:10.1016/j.cyto.2016.09.004

Cited by 51 publications

(29 citation statements)

References 39 publications

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“…Additionally, the cytokines IL-6 and IL-12 are known to upregulate the production of iNOS in macrophages (Jana et al 2003), while IL-12 also promotes NF-κB activation in macrophages (Pahan et al 2001). These cytokines induce the expression of iNOS and NO, and overexpression of proinflammatory mediators can result in tissue injury and multiple organ failure (Amirshahrokhi and Khalili 2016). The upregulated IL-6, IL-12, and TNF-α levels in LPS-induced RAW264.7 cells were significantly decreased with treatment of diosmin compared with control group treated with LPS only.…”

Section: Discussionmentioning

confidence: 99%

Diosmin suppresses the proinflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages via NF-κB and MAPKs signal pathways

Berköz

2019

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Diosmin is an unsaturated flavonoid glycoside, presents in citrus fruits. The aim of this study is to investigate the molecular mechanism of diosmin with respect to the NF-κB and MAPKs signaling pathways. Firstly, 10, 20, 30, 40 and 50 µM diosmin were treated to lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. The anti-inflammatory effects of diosmin was displayed via measuring prostaglandin E 2 (PGE 2), nitric oxide (NO), interleukines (IL-6, IL-12), tumor necrosis factor α (TNF-α) production, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), IL-6, IL-12, TNF-α mRNA levels, and phosphorylation levels of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκB-α) and mitogen-activated protein kinases (MAPKs); JNK, ERK, and p38 in LPS induced RAW264.7 macrophages. Our study showed that especially high concentrations of diosmin decreased NO, PGE 2 , IL-6, IL-12, TNF-α production and mRNA levels of these mediators (p < 0.05). The expression of phosphorylated-JNK was significantly suppressed by diosmin at 40 and 50 µM concentrations. Furthermore, diosmin significantly inhibited the expression of phosphorylated-ERK, p38, and p-IκB-α in a dose-dependent manner. Our results suggest that diosmin is a potent anti-inflammatory agent and has potential for development into a therapeutic agent for inflammation-associated disorders.

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Section: Discussionmentioning

confidence: 99%

Diosmin suppresses the proinflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages via NF-κB and MAPKs signal pathways

Berköz

2019

gpb

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“…Other studies also reported that carvedilol can reduce serum TNF production and is able to suppress the CD107a and HLA-DR on circulating cytotoxic T cells, all compounds critical to the pathogenesis of chronic heart failure [23, 30–32]. Besides, this beta-blocker also interferes with intracellular signaling proteins (e.g., NF- κ B, Src-ERK) and with the expression of chemokines (e.g., CCL2) in experimental and noncardiac study models [33, 34]. …”

Section: Discussionmentioning

confidence: 99%

Potential Role of Carvedilol in the Cardiac Immune Response Induced by Experimental Infection with Trypanosoma cruzi

Horta

Leite

Costa

et al. 2017

BioMed Research International

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Trypanosoma cruzi causes a cardiac infection characterized by an inflammatory imbalance that could become the inciting factor of the illness. To this end, we evaluated the role of carvedilol, a beta-blocker with potential immunomodulatory properties, on the immune response in C57BL/6 mice infected with VL-10 strain of T. cruzi in the acute phase. Animals (n = 40) were grouped: (i) not infected, (ii) infected, (iii) infected + carvedilol, and (iv) not infected + carvedilol. We analyzed parameters related to parasitemia, plasma levels of TNF, IL-10, and CCL2, and cardiac histopathology after the administration of carvedilol for 30 days. We did not observe differences in the maximum peaks of parasitemia in the day of their detection among the groups. The plasma TNF was elevated at 60 days of infection in mice treated or not with carvedilol. However, we observed a decreased CCL2 level and increased IL-10 levels in those infected animals treated with carvedilol, which impacted the reduction of the inflammatory infiltration in cardiac tissue. For this experimental model, carvedilol therapy was not able to alter the levels of circulating parasites but modulates the pattern of CCL2 and IL-10 mediators when the VL10 strain of T. cruzi was used in C57BL6 mice.

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“…Some cytokines, including TNF-a, IL-6, and IL-8 were reported as clinically relevant therapeutic targets in PQ-induced inammation. 30,31 It has reported that the reduced levels of these pro-inammatory cytokines found to decrease the severity of PQ-induced lung injury. 32 S100A8 and S100A9, which are members of the alarmin family that are released into the extracellular space upon infection or tissue injury, were reported to lead to the production of TNF-a and other cytokines.…”

Section: Discussionmentioning

confidence: 99%

Identification of potential serum biomarkers of acute paraquat poisoning in humans using an iTRAQ quantitative proteomic

et al. 2018

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Carvedilol attenuates paraquat-induced lung injury by inhibition of proinflammatory cytokines, chemokine MCP-1, NF-κB activation and oxidative stress mediators

Cited by 51 publications

References 39 publications

Diosmin suppresses the proinflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages via NF-κB and MAPKs signal pathways

Diosmin suppresses the proinflammatory mediators in lipopolysaccharide-induced RAW264.7 macrophages via NF-κB and MAPKs signal pathways

Potential Role of Carvedilol in the Cardiac Immune Response Induced by Experimental Infection with Trypanosoma cruzi

Identification of potential serum biomarkers of acute paraquat poisoning in humans using an iTRAQ quantitative proteomic

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