Phyllolobium chinense Fisch Flavonoids (PCFF) Suppresses the M1 Polarization of LPS-Stimulated RAW264.7 Macrophages by Inhibiting NF-κB/iNOS Signaling Pathway

Fan, Hua; Wu, Qiong; Peng, Longping; Du, Li; Dong, Yidan; Cao, Min; Liu, Ping; Wang, Xu; Hu, Xudong; Wang, Youhua

doi:10.3389/fphar.2020.00864

Cited by 20 publications

(16 citation statements)

References 26 publications

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“…Therefore, reductions in NO level as observed in our results suggest that flavonoids fractions nullified the production of NO by inhibiting the expression of iNOS [54]. Fan et al [55] showed that flavonoids derived from Phyllolobium chinense produced similar NO-lowering effect by specific inhibition of iNOS in Zebrafish model. Malondialdehyde (MDA), an index of oxidative damage to lipids [13], increased dramatically in the plasma, liver and the kidneys of the arsenic exposed group (Fig.…”

Section: Discussionsupporting

confidence: 64%

Flavonoid-rich fractions from Clerodendrum volubile and Vernonia amygdalina extenuates arsenic-invoked hepato-renal toxicity via augmentation of the antioxidant system in rats

Ugbaja

Akinhanmi

Ugwor

et al. 2021

Clinical Nutrition Open Science

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Arsenicosis remains a global health concern due to devastating health effects. Clerodendrum volubile and vernonia amygdalina have tremendous bioactivities against oxidative stress-related diseases. The study, therefore, appraised the effects of flavonoids fractions from C. volubile and V. amygdalina (FCV and FVA respectively) against arsenic-induced oxidative stress in rats. Thirty male Wistar rats (120 ± 10 g) were divided into six groups of five each; Control (distilled water), arsenic alone (40 ppm sodium arsenite), arsenic þ FCV (100 mg/kg), arsenic þ FVA (100 mg/kg), arsenic þ FCV and FVA (50 mg/kg each), and arsenic þ vitamin C (100 mg/kg). The treatment commenced after four-week long arsenic exposure and lasted another four weeks. Blood, liver and kidneys of the rats were collected after sacrifice following an overnight fast. Arsenic caused significant (p<0.05) reductions in the total thiols levels in the plasma, liver, and kidneys, as well as the lowering of catalase and glutathione peroxidase activities.

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Section: Discussionsupporting

confidence: 64%

Flavonoid-rich fractions from Clerodendrum volubile and Vernonia amygdalina extenuates arsenic-invoked hepato-renal toxicity via augmentation of the antioxidant system in rats

Ugbaja

Akinhanmi

Ugwor

et al. 2021

Clinical Nutrition Open Science

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“…The results of immunocytochemistry suggested that MBVP cells were PDGFRβ + cells and could be used as the PDGFRβ + pericytes model in vitro (Figure 3A). In addition, we induced and identified M1 or M2 polarization of macrophages according to previous reports (Kigerl et al, 2009;Hiroi et al, 2013;Fan et al, 2020). The results of Western blot showed that compared with other groups, M1 macrophages significantly expressed iNOS while M2 macrophages significantly expressed CD206 (p < 0.0001 for iNOS, p < 0.001 for CD206, Figures 3B-D).…”

Section: Identification Of Pdgfrβ + Pericytes and Macrophages Polarization In Vitromentioning

confidence: 89%

M2 Macrophages Promote PDGFRβ+ Pericytes Migration After Spinal Cord Injury in Mice via PDGFB/PDGFRβ Pathway

Zheng

et al. 2021

Front. Pharmacol.

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Platelet derived growth factor receptor β positive (PDGFRβ+) pericytes form fibrotic scar, which prevents axonal regeneration after spinal cord injury (SCI). However, the mechanism by which PDGFRβ+ pericytes migrate to the injury core is unclear. Here, we investigated the effect and mechanism of macrophages polarization on PDGFRβ+ pericytes migration after SCI. Macrophages were closely related to the spatiotemporal distribution of PDGFRβ+ pericytes in the injury core at 3, 7, and 14 days postinjury (dpi). Macrophages appeared M2 polarization at 3 and 7 dpi while M1 polarization at 14 dpi. The expression of platelet derived growth factor B (PDGFB) was significantly increased after SCI and after macrophages M2 polarization. The promoting effect of exogenous PDGFB and M2 macrophages conditioned medium on PDGFRβ+ pericytes migration could be blocked by SU16f, a PDGFRβ specific inhibitor. These findings indicate that M2 macrophages can secrete PDGFB acting on PDGFRβ to promote PDGFRβ+ pericytes migration, which can be blocked by a PDGFRβ specific inhibitor SU16f. The PDGFB/PDGFRβ pathway is a promising new target for the treatment of SCI.

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“…Here, we investigated whether also macrophage cell population might be targeted by A. tonkinensis decoction and by its major component TAT-2, assessing if they could interfere in macrophage acquisition of a pro-inflammatory phenotype, and decrease formation of osteoclasts, key cells in the RA pathologic joint damage. Using the established inflammation in vitro model of RAW264.7 macrophage cell line conditioned with LPS (Fan et al, 2020), we investigated the effects on nitric oxide (NO) and IL-6 production. Moreover, inducing osteoclastogenesis in RAW264.7 by RANKL protein (Kim et al, 2019), we evaluated the inhibition of osteoclast differentiation process and the decrease of its markers, also exploring the interference at RANK signaling level.…”

Section: Introductionmentioning

confidence: 99%

Artocarpus tonkinensis Extract Inhibits LPS-Triggered Inflammation Markers and Suppresses RANKL-Induced Osteoclastogenesis in RAW264.7

et al. 2021

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Artocarpus tonkinensis (At) leaf decoction, a traditional remedy prepared in North Vietnam by the Hmong ethnic group, is a tea extract rich in bioactive compounds that may have therapeutic effects in arthritis and backache. Indeed, it has been demonstrated that At is able to inhibit Th17 lymphocytes development and to protect mice in an experimental model of collagen-induced arthritis. By resorting to macrophage in vitro models of inflammation and osteoclastogenesis, we showed that At extract significantly reduced nitric oxide synthase 2 (NOS2) activity and IL-6 production by RAW 264.7 murine cells. Moreover, At demonstrated an anti-osteoclastogenic effect, as revealed by complete inhibition of TRAP-positive osteoclast formation and decreased expression of key osteoclast-related genes. This At activity likely relies on the inhibition of RANK downstream signaling pathway, as the activation of non-receptor tyrosine kinase Src is reduced upon RANKL-At exposure. Protective effect of At against bone loss was also enlightened in vivo by collagen-induced arthritis (CIA) experiment demonstrating that, although paw edema was only weakly opposed by drinking At decoction, bone and cartilage were well preserved in CIA+At mice and joint tissue expressed decreased levels of osteoclast marker genes respect to CIA control group. Maesopsin 4-O-β-D-glucoside (i.e., TAT-2, one of the main decoction bioactive components) was capable to contrast NOS2 activity, IL-6 expression and osteoclast formation, too, albeit to a lesser extent when compared to At decoction. Overall, this study enlightens another At cell target, macrophages, beside Th17 lymphocytes, and suggests that the anti-arthritic beneficial effects of At decoction largely derives from its ability to counteract not only inflammation, but also osteoclastogenesis.

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Phyllolobium chinense Fisch Flavonoids (PCFF) Suppresses the M1 Polarization of LPS-Stimulated RAW264.7 Macrophages by Inhibiting NF-κB/iNOS Signaling Pathway

Cited by 20 publications

References 26 publications

Flavonoid-rich fractions from Clerodendrum volubile and Vernonia amygdalina extenuates arsenic-invoked hepato-renal toxicity via augmentation of the antioxidant system in rats

Flavonoid-rich fractions from Clerodendrum volubile and Vernonia amygdalina extenuates arsenic-invoked hepato-renal toxicity via augmentation of the antioxidant system in rats

M2 Macrophages Promote PDGFRβ+ Pericytes Migration After Spinal Cord Injury in Mice via PDGFB/PDGFRβ Pathway

Artocarpus tonkinensis Extract Inhibits LPS-Triggered Inflammation Markers and Suppresses RANKL-Induced Osteoclastogenesis in RAW264.7

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