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Cordycepin Suppresses Expression of Diabetes Regulating Genes by Inhibition of Lipopolysaccharide-induced Inflammation in Macrophages.

Shin S, Lee S, Kwon J, Moon S, Lee S, Lee CK, Cho K, Ha NJ, Kim K - Immune Netw (2009)

Bottom Line: In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells.T2D regulating genes such as 11beta-HSD1 and PPARgamma were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration.Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-kappaB dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Sahmyook University, Seoul, Korea.

ABSTRACT

Background: It has been recently noticed that type 2 diabetes (T2D), one of the most common metabolic diseases, causes a chronic low-grade inflammation and activation of the innate immune system that are closely involved in the pathogenesis of T2D. Cordyceps militaris, a traditional medicinal mushroom, produces a component compound, cordycepin (3'-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immunological stimulating, anti-cancer, and anti-infection activities. The molecular mechanisms of cordycepin in T2D are not clear. In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells.

Methods: We confirmed the levels of diabetes regulating genes mRNA and protein of cytokines through RT-PCR and western blot analysis and followed by FACS analysis for the surface molecules.

Results: Cordycepin inhibited the production of NO and pro-inflammatory cytokines such as IL-1beta, IL-6, and TNF-alpha in LPS-activated macrophages via suppressing protein expression of pro-inflammatory mediators. T2D regulating genes such as 11beta-HSD1 and PPARgamma were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration. In accordance with suppressed pro-inflammatory cytokine production lead to inhibition of diabetic regulating genes in activated macrophages. Cordycepin suppressed NF-kappaB activation in LPS-activated macrophages.

Conclusion: Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-kappaB dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.

No MeSH data available.


Related in: MedlinePlus

Effect of cordycepin on NF-κB activation. Levels of NF-κB protein in RAW 264.7 cells. Cells were incubated with various concentrations of cordycepin in the presence of LPS (100 ng/ml) overnight. Protein from each sample was resolved in 12% SDS-PAGE and then analyzed by Western blotting. β-actin was used in as a control.
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Figure 6: Effect of cordycepin on NF-κB activation. Levels of NF-κB protein in RAW 264.7 cells. Cells were incubated with various concentrations of cordycepin in the presence of LPS (100 ng/ml) overnight. Protein from each sample was resolved in 12% SDS-PAGE and then analyzed by Western blotting. β-actin was used in as a control.

Mentions: To investigate whether cordycepin could affect nuclear translocation of NF-κB, western blot analysis for NF-κB p65 was carried out with cell lysate in macrophages (Fig. 6). Amount of NF-κB p65 was markedly increased upon exposure to LPS alone, but cordycepin decreased NF-κB p65.


Cordycepin Suppresses Expression of Diabetes Regulating Genes by Inhibition of Lipopolysaccharide-induced Inflammation in Macrophages.

Shin S, Lee S, Kwon J, Moon S, Lee S, Lee CK, Cho K, Ha NJ, Kim K - Immune Netw (2009)

Effect of cordycepin on NF-κB activation. Levels of NF-κB protein in RAW 264.7 cells. Cells were incubated with various concentrations of cordycepin in the presence of LPS (100 ng/ml) overnight. Protein from each sample was resolved in 12% SDS-PAGE and then analyzed by Western blotting. β-actin was used in as a control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2803303&req=5

Figure 6: Effect of cordycepin on NF-κB activation. Levels of NF-κB protein in RAW 264.7 cells. Cells were incubated with various concentrations of cordycepin in the presence of LPS (100 ng/ml) overnight. Protein from each sample was resolved in 12% SDS-PAGE and then analyzed by Western blotting. β-actin was used in as a control.
Mentions: To investigate whether cordycepin could affect nuclear translocation of NF-κB, western blot analysis for NF-κB p65 was carried out with cell lysate in macrophages (Fig. 6). Amount of NF-κB p65 was markedly increased upon exposure to LPS alone, but cordycepin decreased NF-κB p65.

Bottom Line: In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells.T2D regulating genes such as 11beta-HSD1 and PPARgamma were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration.Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-kappaB dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.

View Article: PubMed Central - PubMed

Affiliation: College of Pharmacy, Sahmyook University, Seoul, Korea.

ABSTRACT

Background: It has been recently noticed that type 2 diabetes (T2D), one of the most common metabolic diseases, causes a chronic low-grade inflammation and activation of the innate immune system that are closely involved in the pathogenesis of T2D. Cordyceps militaris, a traditional medicinal mushroom, produces a component compound, cordycepin (3'-deoxyadenosine). Cordycepin has been known to have many pharmacological activities including immunological stimulating, anti-cancer, and anti-infection activities. The molecular mechanisms of cordycepin in T2D are not clear. In the present study, we tested the role of cordycepin on the anti-diabetic effect and anti-inflammatory cascades in LPS-stimulated RAW 264.7 cells.

Methods: We confirmed the levels of diabetes regulating genes mRNA and protein of cytokines through RT-PCR and western blot analysis and followed by FACS analysis for the surface molecules.

Results: Cordycepin inhibited the production of NO and pro-inflammatory cytokines such as IL-1beta, IL-6, and TNF-alpha in LPS-activated macrophages via suppressing protein expression of pro-inflammatory mediators. T2D regulating genes such as 11beta-HSD1 and PPARgamma were decreased as well as expression of co-stimulatory molecules such as ICAM-1 and B7-1/-2 were also decreased with the increment of its concentration. In accordance with suppressed pro-inflammatory cytokine production lead to inhibition of diabetic regulating genes in activated macrophages. Cordycepin suppressed NF-kappaB activation in LPS-activated macrophages.

Conclusion: Based on these observations, cordycepin suppressed T2D regulating genes through the inactivation of NF-kappaB dependent inflammatory responses and suggesting that cordycepin will provide potential use as an immunomodulatory agent for treating immunological diseases.

No MeSH data available.


Related in: MedlinePlus