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Sweetpotato Leaves Inhibit Lipopolysaccharide-Induced Inflammation in RAW 264.7 Macrophages via Suppression of NF-κB Signaling Pathway.

ABSTRACT: Limited information is available regarding the health-promoting activities of sweetpotato leaves (SPL). The present study investigated antioxidant and anti-inflammatory effects, and phenolic contents in 29 SPL cultivars harvested in 2018 and 2019. Extracts showed total phenolic contents 9.4-23.1 mg gallic acid equivalent/g, and DPPH radical scavenging activity indicated 36.6-247.3 mM of Trolox equivalent/g. SPL extracts were identified to contain bioactive components such as, chlorogenic acid (11.7-22.1 μg/mg), 3,4-dicaffeoylquinic acid (16.3-59.9 μg/mg), 3,5-dicaffeoylquinic acid (50.9-72.7 μg/mg), chlorophyll B (6.1-12.3 μg/mg), lutein (1.9-4.9 μg/mg), chlorophyll A (2.7-4.3 μg/mg) and β-carotene (0.1 ≤ μg/mg). RAW 264.7 murine macrophage cells were pretreated with 100-200 μg/mL of SPL extracts and 20 μM of dexamethasone, and inflammation was stimulated by lipopolysaccharide (LPS, 100 ng/mL) treatment for 24 h. In LPS-treated cells, prostaglandin E2 production and COX-2 expression were not downregulated by pretreatment of SPL extracts. However, SPL pretreated cells showed significant suppression of nitric oxide (NO), TNF-α, and IL-1β levels under the LPS-induced inflammatory condition. In addition, SPL extracts induced an anti-inflammatory effect in LPS-stimulated RAW 264.7 cells through suppression of NF-κB nuclear translocation, IKK-α and IκB-α phosphorylation, and iNOS expression. These results indicate that SPL extract can be utilized as a functional food ingredient.

SUBMITTER: Cho HD

PROVIDER: S-EPMC8464942 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Lithium remains the preferred Food and Drug Administration- (FDA-) approved psychiatric drug for treatment of bipolar disorders since its medical establishment more than half a century ago. Recent studies revealed a promising role for lithium in the regulation of inflammation, oxidative stress, and neurodegeneration albeit unclear about its exact mode of action. Thus, the intention of this study is to delineate the regulatory mechanisms of lithium on oxidative stress in lipopolysaccharide- (LPS-) activated macrophages by evaluating its effects on nuclear factor-κB (NF-κB) activity and mRNA expression of multiple oxidative stress-related NF-κB genes. Raw 264.7 macrophages were treated with up to 10 mM lithium, and no change in cell proliferation, viability, growth, and cell adhesion was observed in real time. Pretreatment with low doses of lithium was shown to reduce nitric oxide (NO) production in LPS-activated macrophages. A reduced internal H2DCFDA fluorescence intensity, indicative of reduced reactive oxygen species (ROS) production, was observed in LPS-activated Raw 264.7 macrophages treated with lithium. Lithium has been shown to lower the production of the chemokine RANTES; furthermore, this inhibitory action of lithium has been suggested to be independent of glycogen synthase kinase-3 β (GSK3β) activity. It is shown here that lithium modulates the expression of several inflammatory genes including IκB-α, TRAF3, Tollip, and NF-κB1/p50 which are regulators of the NF-κB pathway. Moreover, lithium inhibits NF-κB activity by lowering nuclear translocation of NF-κB in LPS-activated macrophages. This is the first study to associate Tollip, Traf-3, and IκB-α mRNA expression with lithium effect on NF-κB activity in LPS-activated Raw 264.7 macrophages. Although these effects were obtained using extratherapeutic concentrations of lithium, results of this study provide useful information towards understanding the mode of action of lithium. This study associates lithium with reduced oxidative stress in LPS-activated Raw 264.7 macrophages and further suggests candidate molecular targets for the regulation of oxidative stress-related diseases using lithium beyond bipolar disorders.

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Sweetpotato Leaves Inhibit Lipopolysaccharide-Induced Inflammation in RAW 264.7 Macrophages via Suppression of NF-κB Signaling Pathway.

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