International immunopharmacology
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Int. Immunopharmacol. · Nov 2016
Cnidilide, an alkylphthalide isolated from the roots of Cnidium officinale, suppresses LPS-induced NO, PGE2, IL-1β, IL-6 and TNF-α production by AP-1 and NF-κB inactivation in RAW 264.7 macrophages.
Cnidilide, an alkyl phthalide isolated from the rhizome of Cnidium officinale, has been reported to possess antispasmodic and sedative effects. However, the anti-inflammatory capacity and molecular mechanism of cnidilide have not been studied to date. In the present study, we investigated the inhibitory effects of cnidilide on LPS-induced pro-inflammatory mediators and the underlying molecular mechanisms in RAW 264.7 macrophages. ⋯ In addition, cnidilide inhibited LPS-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and mitogen- and stress-activated protein kinase 1(MSK-1), a downstream kinase. Moreover, the phosphorylation of c-Jun N-terminal kinase (JNK) was suppressed by cnidilide in a concentration-dependent manner, whereas it did not inhibit the extracellular signal-regulated kinase (ERK) phosphorylation in LPS-stimulated RAW 264.7 macrophages. Taken together, our findings suggest that cnidilide has anti-inflammatory properties by inhibiting p38 MAPK, JNK, AP-1, and the NF-κB pathway in LPS-stimulated RAW 264.7 macrophages.
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Int. Immunopharmacol. · Sep 2016
Genipin alleviates LPS-induced acute lung injury by inhibiting NF-κB and NLRP3 signaling pathways.
Genipin has been reported to have anti-inflammatory effect. However, its role on lipopolysaccharide (LPS)-induced acute lung injury (ALI) has not been explored. This study aimed to evaluate the effect of genipin on murine model of acute lung injury induced by LPS. ⋯ Moreover, it also inhibited the levels of TNF-α, IL-1β, IL-6 in the BALF. In addition, genipin significantly inhibited LPS-induced NF-κB and NLRP3 activation. In conclusion, these results demonstrate that genipin protected against LPS-induced ALI through inhibiting NF-κB and NLRP3 signaling pathways.
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Int. Immunopharmacol. · Sep 2016
Resokaempferol-mediated anti-inflammatory effects on activated macrophages via the inhibition of JAK2/STAT3, NF-κB and JNK/p38 MAPK signaling pathways.
The excessive or prolonged production of inflammatory mediators can result in numerous chronic diseases, such as rheumatoid arthritis, atherosclerosis, diabetes, and cancer. Therefore, for many inflammatory-related diseases, pharmaceutical intervention is required to restrain the excessive release of such inflammatory mediators. Novel therapeutics and mechanistic insight are sought for the management of chronic inflammatory diseases. ⋯ RES also inhibited the activation of NF-κB and JNK/p38 MAPK signaling pathways in LPS-induced RAW264.7 cells. Additionally, RES inhibited the activation of the JAK2/STAT3 pathway in exogenous IL-6-activated RAW264.7 macrophages. We conclude that RES inhibits the inflammatory response in activated macrophages by blocking the activation of the JAK2/STAT3 pathway by both LPS and IL-6 signaling.
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Int. Immunopharmacol. · Sep 2016
Lectin from Abelmoschus esculentus reduces zymosan-induced temporomandibular joint inflammatory hypernociception in rats via heme oxygenase-1 pathway integrity and tnf-α and il-1β suppression.
Temporomandibular joint (TMJ) disorders show inflammatory components, heavily impacting on quality of life. Abelmoschus esculentus is largely cultivated in Northeastern Brazil for medicinal purposes, having it shown anti-inflammatory activity. We evaluated A. esculentus lectin (AEL) efficacy in reducing zymosan-induced temporomandibular joint inflammatory hypernociception in rats along with the mechanism of action through which it exerts anti-inflammatory activity. ⋯ AEL reduced TNF-α and IL-1β levels in TMJ tissue and trigeminal ganglion. AEL effects, however, were not observed in the presence of ZnPP-IX. These findings suggest that AEL efficacy depends on TNF-α/IL-1β inhibition and HO-1 pathway integrity.
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Int. Immunopharmacol. · Sep 2016
Berberine alleviates postoperative cognitive dysfunction by suppressing neuroinflammation in aged mice.
Postoperative cognitive dysfunction (POCD) is a significant cause of morbidity after surgery, especially for the elderly. Accumulating evidence has demonstrated that neuroinflammation plays a key role in the pathogenesis of POCD. Thus, we hypothesized that berberine, an isoquinoline alkaloid with anti-inflammatory effects, could improve surgery-induced cognitive impairment. ⋯ Notably, berberine treatment rescued surgery-induced cognitive impairment and inhibited the release of IBA1, IL-1β, and IL-6 in the hippocampus. In line with the in vivo study, berberine treatment suppressed LPS-stimulated production of TNF-α and IL-1β in BV2 cells. In conclusion, our study suggests that berberine could alleviate POCD by suppressing neuroinflammation in aged mice.