Curcumin Protects Mice From Coxsackievirus B3-Induced Myocarditis by Inhibiting the Phosphatidylinositol 3 kinase/Akt/Nuclear Factor-κB Pathway

Song, Yanting; Ge, Wen; Cai, HaiBing; Zhang, Haichen

doi:10.1177/1074248413503044

Cited by 39 publications

(23 citation statements)

References 40 publications

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“…Moreover, a systemic and myocardial reduction in these cytokines, and ultimately NF-κ-β, was also seen following administration of curcumin in Coxsackievirus-infected mice (Song et al. 2013 ). Although we did not analyze the NF-κ-B pathway in this study, we think that the biological effects of curcumin could be due to the inhibition of this transcription factor during the inflammatory process.…”

Section: Discussionmentioning

confidence: 97%

Curcumin suppresses inflammatory cytokines and heat shock protein 70 release and improves metabolic parameters during experimental sepsis

Silva

Catalão

Felippotti

et al. 2016

Pharmaceutical Biology

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Context: Curcumin has been reported to have anti-inflammatory, antioxidant and hypoglycaemic properties, besides reducing mortality in sepsis.Objective: This study evaluates the biological activities of a curcumin dispersion formulated by spray-drying in experimental sepsis.Materials and methods: Male Wistar rats were subjected to sepsis by caecal ligation and puncture (CLP), controls were sham operated. The animals were treated with curcumin dispersion (100 mg/kg, p.o.) or water for 7 days prior to CLP and at 2 h after surgery. One group was used to analyze curcumin absorption through HPLC; another had the survival rate assessed during 48 h; and from a third group, blood was collected by decapitation to analyze metabolic and inflammatory parameters.Results: The plasma curcumin levels reached 2.5 ng/mL at 4 h, dropped significantly (p < 0.001) at 6 h (1.2 ng/mL), and were undetectable at 24 h in both groups. Curcumin temporarily increased the survival rate of the septic rats by 20%. Moreover, it attenuated glycaemia (p < 0.05) and volemia (p < 0.05) alterations typically observed during sepsis, and decreased the levels of the proinflammatory cytokines IL-1β and IL-6 in plasma (p < 0.001) and peritoneal lavage fluid (p < 0.05) of septic rats. Serum HSP70 levels were decreased (p < 0.01) at 24 h after CLP.Discussion and conclusion: Our results show that the curcumin dispersion dose employed was not detrimental to the septic rats. In fact, it temporarily increased their survival rate, improved important metabolic parameters, reduced proinflammatory cytokines and HSP70 production.

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Section: Discussionmentioning

confidence: 97%

Curcumin suppresses inflammatory cytokines and heat shock protein 70 release and improves metabolic parameters during experimental sepsis

Silva

Catalão

Felippotti

et al. 2016

Pharmaceutical Biology

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“…In addition, CMN showed noticeable resistance to cardiac hypertrophy caused by banding of the aorta, and the progression of heart failure was decreased by NF-κB activation and monocyte chemoattractant protein-1 (MCP-1), IL-6, IL-1β, and TNF-α mRNA and protein expression induced by aortic banding ( 37 ). Also, Song et al ( 38 ) demonstrated that CMN reduces the systemic and local expressions of NF-κB, IL-6, and IL-1β in the myocardium as evidenced by ameliorated symptoms of myocarditis. In a different study by Wang et al ( 39 ), CMN downregulated the levels of proinflammatory cytokines in the ischemic heart, which is concomitant with reduced TNF-α and IL-6 levels, infarct size, and ameliorated ischemic injury.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of curcumin and beta-carotene on cisplatin-induced cardiotoxicity: An experimental rat model

Bahadir

Ceyhan²,

Ö³

et al. 2018

Anatol J Cardiol

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ObjectiveCisplatin (CDDP) has been known to be an effective antineoplastic drug; however, it has a cardiotoxic effect. Curcumin (CMN) and beta-carotene (BC) have been suggested to protect biological systems against CDDP-induced damage. The current study was conducted to evaluate the possible protective roles of CMN and BC on CDDP-induced cardiotoxicity in rat cardiac tissues.MethodsA total of 49 adult femaleWistar albino rats were equally divided into seven groups as followscontrol (no medication), sesame oil (1 mg/kg), CDDP (single dose injection two times as once a week, 5 mg/kg/week), BC (100 mg/kg), CDDP+BC (pretreated BC for 30 min before CDDP injection), CMN (200 mg/kg), and CDDP+CMN (pretreated CMN for 30 min before CDDP injection). These treatments were applied intraperitoneally for CDDP and with gavage for CMN and BC. The oxidative/antioxidant indicators, inflammatory cytokines, and histopathological alterations were examined.ResultsThese alterations included a marked increase in malondialdehyde (MDA) level, significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities, and significant elevation of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6 in the CDDP group compared with the other groups. Histopathologically, CDDP-induced severe myocardial degenerative changes were observed. However, the CDDP-induced disturbances in the above-mentioned parameters significantly improved by treatment with BC and particularly CMN.ConclusionThis study indicated that CDDP treatment markedly caused cardiotoxicity; however, treatment with CMN or BC ameliorated this cardiotoxicity in rats. Furthermore, these findings revealed that treatment with CMN has a higher cardioprotective effect than that with BC against CDDP-induced cardiotoxicity in rat cardiac tissues.

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“…Apoptosis response is an important pathophysiological change in the early stage of myocardial I/R that further leads to severe heart failure . Apoptosis, necrosis, and autophagic cell death are possibly the final arbiters of cardiomyocyte numbers following AMI; cell apoptosis may be associated with a variety of damaging stimuli, particularly continuous I/R . Therefore, the inhibition of cardiomyocyte apoptosis is particularly important for reducing myocardial I/R damage.…”

Section: Discussionmentioning

confidence: 99%

Baicalin attenuates myocardial ischemia‐reperfusion injury through Akt/NF‐κB pathway

Luan

Sun

Wang

et al. 2018

J of Cellular Biochemistry

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Background: Baicalin can attenuate myocardial ischemia-reperfusion (I/R) on damage. However, the mechanisms are still not fully understood. The study aimed to investigate the antiapoptosis and anti-inflammatory effects of baicalin on myocardial I/R-induced injury. Methods:We established male rats I/R model, and baicalin was intragastric administration after ischemia onset. All experimental animals were randomly divided into five groups: group I, sham; group II, I/R; group III, 50 mg/kg; group IV, 100 mg/kg; and group V, 200 mg/kg baicalin. Postoperation, left ventricular (LV) function was recorded by transthoracic echocardiography. Myocardial infarct size, number of vessels and apoptosis were detected by histology and immunohistochemistry. Furthermore, the messenger RNA (mRNA) and protein levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), IL-6, IL-8, IL-10, Bcl2, Bax, caspase-3, phosphatidylinositol 3-kinase (PI3K), Akt, p-Akt, and nuclear factor-κB (NF-κB) p65 in myocardial tissues were measured by quantitative real-time polymerase chain reaction and Western blot analysis assays. Result: When compared with I/R groups, baicalin could significantly improve LV hemodynamic parameters. Myocardial infarct size and apoptosis were significantly decreased, but the vessel density was increased. The mRNA levels of TNF-α, IL-1β, IL-6, and IL-8 were downregulated, but the levels of IL-10, proapoptotic genes caspase-3, and the ratio of Bax/Bcl2 were upregulated. Moreover, the protein expression of PI3K, p-Akt, and Akt were upregulated but NF-κB p65 was downregulated in the groups III, IV, and V than in group II. Conclusion:Our current study suggested that baicalin attenuated myocardial I/R-induced damage, inhibited myocardial apoptosis, and inflammation by activating PI3K/Akt but suppressing NF-κB signaling. K E Y W O R D S apoptosis, baicalin, ischemia-reperfusion, inflammation, PI3K/Akt/NF-κB signaling J Cell Biochem. 2019;120:3212-3219. wileyonlinelibrary.com/journal/jcb 3212 |

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Curcumin Protects Mice From Coxsackievirus B3-Induced Myocarditis by Inhibiting the Phosphatidylinositol 3 kinase/Akt/Nuclear Factor-κB Pathway

Cited by 39 publications

References 40 publications

Curcumin suppresses inflammatory cytokines and heat shock protein 70 release and improves metabolic parameters during experimental sepsis

Curcumin suppresses inflammatory cytokines and heat shock protein 70 release and improves metabolic parameters during experimental sepsis

Protective effects of curcumin and beta-carotene on cisplatin-induced cardiotoxicity: An experimental rat model

Baicalin attenuates myocardial ischemia‐reperfusion injury through Akt/NF‐κB pathway

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