Catalpol suppresses advanced glycation end-products-induced inflammatory responses through inhibition of reactive oxygen species in human monocytic THP-1 cells

Choi, Hee‐Jung; Jang, Hye-Jin; Chung, Tae‐Wook; Jeong, Seung-Il; Cha, Jaeho; Choi, Jun-Young; Han, Chang Woo; Jang, Yong-Suk; Joo, Myungsoo; Jeong, Hyein; Ha, Ki‐Tae

doi:10.1016/j.fitote.2013.01.014

Cited by 56 publications

(41 citation statements)

References 60 publications

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“…Therefore, investigating the interaction between AGEs and the polarization of macrophages might further reveal the underlying mechanism of diabetic accelerated atherosclerosis. Previous studies have shown that AGEs not only promoted macrophages to secret proinflammatory cytokines [19, 20] but also enhanced their migration ability [21], while Choi et al recently proved that AGEs enhanced iNOS expression in macrophages [22]. In the present study, we also found AGEs upregulated iNOS production.…”

Section: Discussionsupporting

confidence: 79%

Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway

Jin

Yao

Zhou

et al. 2015

BioMed Research International

151

116

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Atherosclerotic lesions are accelerated in patients with diabetes. M1 (classically activated in contrast to M2 alternatively activated) macrophages play key roles in the progression of atherosclerosis. Since advanced glycation end products (AGEs) are major pathogenic factors and active inflammation inducers in diabetes mellitus, this study assessed the effects of AGEs on macrophage polarization. The present study showed that AGEs significantly promoted macrophages to express IL-6 and TNF-α. M1 macrophage markers such as iNOS and surface markers including CD11c and CD86 were significantly upregulated while M2 macrophage markers such as Arg1 and CD206 remained unchanged after AGEs stimulation. AGEs significantly increased RAGE expression in macrophages and activated NF-κB pathway, and the aforementioned effects were partly abolished by administration of anti-RAGE antibody or NF-κB inhibitor PDTC. In conclusion, our results suggest that AGEs enhance macrophage differentiation into proinflammatory M1 phenotype at least partly via RAGE/NF-κB pathway activation.

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Section: Discussionsupporting

confidence: 79%

Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway

Jin

Yao

Zhou

et al. 2015

BioMed Research International

151

116

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“…To investigate the anti-inflammatory effect of scropolioside B, we preincubated THP-1 cells with the compound for 1 h and subsequently stimulated the cells with LPS or PA. We found that scropolioside B significantly blocked the increase in IL-1 β and TNF- α levels induced by LPS or PA (Figure 1). However, at the concentration of 50 μ mol/L, catalpol did not effectively block expression of IL-1 β and TNF- α , although these anti-inflammatory effects had been reported [24, 25]. These observations suggested that scropolioside B has stronger anti-inflammatory activity compared to catalpol.…”

Section: Resultsmentioning

confidence: 90%

“…In this study, we demonstrated that scropolioside B, an iridoid glycoside containing a catalpol and two phenylpropanoids, was more effective than catalpol in inhibiting the expressions of IL-1 β and TNF- α in THP-1 cells activated by LPS or palmitic acid (Figure 1). Our results suggested that scropolioside B has higher anti-inflammatory activity than catalpol, although some studies have reported that catalpol does demonstrate anti-inflammatory effects at high dose by inhibiting COX-2 activity, TNF- α formation, monocyte chemotactic protein-1 (MCP-1), and nitric oxide production [24, 25]. As shown in Figure 2, the anti-inflammatory effects of scropolioside B were mediated by blocking NF- κ B activity (Figure 2).…”

Section: Discussionmentioning

confidence: 94%

Scropolioside B Inhibits IL-1βand Cytokines Expression through NF-κB and Inflammasome NLRP3 Pathways

Zhu

Zhang

Ling

et al. 2014

Mediators of Inflammation

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Chronic inflammation is associated with various chronic illnesses including immunity disorders, cancer, neurodegeneration, and vascular diseases. Iridoids are compounds with anti-inflammatory properties. However their anti-inflammatory mechanism remains unclear. Here, we report that scropolioside B, isolated from a Tibetan medicine (Scrophularia dentata Royle ex Benth.), blocked expressions of TNF, IL-1, and IL-32 through NF-κB pathway. Scropolioside B inhibited NF-κB activity in a dose-dependent manner with IC50 values of 1.02 μmol/L. However, catalpol, similar to scropolioside B, was not effective in inhibiting NF-κB activity. Interestingly, scropolioside B and catalpol decreased the expression of NLRP3 and cardiolipin synthetase at both the mRNA and protein level. Our results showed that scropolioside B is superior in inhibiting the expression, maturation, and secretion of IL-1β compared to catalpol. These observations provide further understanding of the anti-inflammatory effects of iridoids and highlight scropolioside B as a potential drug for the treatment of rheumatoid arthritis and atherosclerosis.

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“…Catalpol has been shown to have an inhibitory effect on the inflammatory reaction in astrocytes, with inactivation of NF-κB proposed as the major determinant for its anti-inflammatory mechanism [17]. Moreover, catalpol suppresses AGE-mediated inflammation by inhibiting ROS production and NF-κB activity [34]. …”

Section: Resultsmentioning

confidence: 99%

Catalpol Ameliorates Sodium Taurocholate-Induced Acute Pancreatitis in Rats via Inhibiting Activation of Nuclear Factor Kappa B

Xiao

Yin

Fan

et al. 2014

IJMS

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Catalpol, an iridoid glucoside extracted from the traditional Chinese herbal medicine, Rehmannia glutinosa, is reported to exert neuroprotective, anti-inflammatory, anti-tumor and anti-apoptotic effects. The main aim of the present study was to investigate whether catalpol ameliorates experimental acute pancreatitis (AP) induced by sodium taurocholate (STC). AP was induced in rats via retrograde injection of 4% STC (0.1 mL/100 g) into the biliopancreatic duct. Rats were pre-treated with saline or catalpol (50 mg/kg) 2 h before STC injection. At 12, 24 and 48 h after injection, the severity of AP was evaluated using biochemical and morphological analyses. Pretreatment with catalpol led to a significant reduction in serum amylase and lipase activities, pancreatic histological damage, myeloperoxidase (MPO) activity, interleukin (IL)-1β, IL-6 and TNF-α levels, and activation of nuclear factor kappa B (NF-κB). Moreover, administration of catalpol increased the viability of pancreatic acinar cells and inhibited NF-κB expression in vitro. Our results collectively support the potential of catalpol as a highly effective therapeutic agent for treatment of AP.

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Catalpol suppresses advanced glycation end-products-induced inflammatory responses through inhibition of reactive oxygen species in human monocytic THP-1 cells

Cited by 56 publications

References 60 publications

Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway

Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway

Scropolioside B Inhibits IL-1βand Cytokines Expression through NF-κB and Inflammasome NLRP3 Pathways

Catalpol Ameliorates Sodium Taurocholate-Induced Acute Pancreatitis in Rats via Inhibiting Activation of Nuclear Factor Kappa B

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