Wood-cultivated ginseng exerts anti-inflammatory effect in LPS-stimulated RAW264.7 cells

Park, Su Bin; Park, Gwang Hun; Um, Yurry; Kim, Hana; Song, Hun Min; Kim, Nahyun; Jeong, Jin Boo

doi:10.1016/j.ijbiomac.2018.05.039

Cited by 26 publications

(18 citation statements)

References 40 publications

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“…Similarly, Jung et al [39] reported that flower extract of Panax notoginseng attenuates the LPS-induced inflammatory response by blocking the NF-κB signaling pathway in murine macrophages. Wood-cultivated ginseng extract dose-dependently suppressed NO and PGE2, attenuated overexpression of iNOS and COX-2, blocked expression of TNF-α and IL-1β, and inhibited NF-κB activation in LPS-stimulated RAW264.7 cells [45]. In addition, Baek et al [46] reported that the saponin fraction from red ginseng possessed greater ability to inhibit NO production and mRNA expression of inflammatory factor genes, such as iNOS, COX-2, TNF-α, and INF-β, than the non-saponin fraction.…”

Section: Resultsmentioning

confidence: 99%

Phenolic Compounds and Ginsenosides in Ginseng Shoots and Their Antioxidant and Anti-Inflammatory Capacities in LPS-Induced RAW264.7 Mouse Macrophages

Fan

Xue

et al. 2019

IJMS

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We conducted this study for the first time to evaluate changes in the composition and contents of phenolic compounds and ginsenosides in ginseng shoot extracts (GSEs) prepared with different steaming times (2, 4, and 6 h) at 120 °C, as well as their antioxidant and anti-inflammatory activities in lipopolysaccharide (LPS)-induced RAW264.7 mouse macrophages (RAW264.7 cells). The results show that total phenol and flavonoid contents were both significantly higher in steamed versus raw GSEs, and the same trend was found for 2,2′-diphenyl-1-picrylhydrazyl (DPPH•) and 2,2′-azobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS•+) scavenging capacities. Among the 18 ginsenosides quantified using high-performance liquid chromatography (HPLC) with the aid of pure standards, polar ginsenosides were abundant in raw GSEs, whereas less-polar or rare ginsenosides appeared after steaming at 120 °C and increased with steaming time. Furthermore, steamed GSEs exhibited a greater ability to inhibit the production of inflammatory mediators and pro-inflammatory cytokines, such as nitric oxide (NO), interleukin (IL)-6, and tumor necrosis factor (TNF)-α in LPS-induced RAW264.7 cells at the same concentration. Relative expression levels of inducible nitric oxide synthase (iNOS), IL-6, TNF-α, and cyclooxygenase-2 (COX-2) mRNAs were attenuated by the GSEs, probably due to the enrichment of less-polar ginsenosides and enhanced antioxidant activity in steamed GSEs. These findings, combined with correlation analysis, showed that less-polar ginsenosides were major contributors to the inhibition of the overproduction of various inflammatory factors, while the inhibitory effects of total phenols and total flavonoids, and their antioxidant abilities, are also important.

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Section: Resultsmentioning

confidence: 99%

Phenolic Compounds and Ginsenosides in Ginseng Shoots and Their Antioxidant and Anti-Inflammatory Capacities in LPS-Induced RAW264.7 Mouse Macrophages

Fan

Xue

et al. 2019

IJMS

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“…Inflammation has been viewed as an immune response to harmful stimuli, tissue injury, or infection that protects the body from various pathogens, such as bacteria, viruses, and fungi [1,2]. However, prolonged and excessive inflammation induces immune disorders and causes excessive tissue damage, resulting in many diseases, including arthritis, diabetes, cardiovascular disease, and cancer [3,4].…”

Section: Introductionmentioning

confidence: 99%

m6A Reader YTHDF2 Regulates LPS-Induced Inflammatory Response

Feng

et al. 2019

IJMS

155

130

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N6-methyladenosine (m6A) is an abundant mRNA modification that affects multiple biological processes, including those involved in the cell stress response and viral infection. YTH domain family 2 (YTHDF2) is an m6A-binding protein that affects the localization and stability of targeted mRNA. RNA-binding proteins (RBPs) can regulate the stability of inflammatory gene mRNA transcripts, thus participating in the regulation of inflammatory processes. As an RBP, the role of YTHDF2 in the LPS-induced inflammatory reaction has not been reported. To elucidate the function of YTHDF2 in the inflammatory response of macrophages, we first detected the expression level of YTHDF2 in RAW 264.7 cells, and found that it was upregulated after LPS stimulation. YTHDF2 knockdown significantly increased the LPS-induced IL-6, TNF-α, IL-1β, and IL-12 expression and the phosphorylation of p65, p38, and ERK1/2 in NF-κB and MAPK signaling. Moreover, the upregulated expression of TNF-α and IL-6 in cells with silenced YTHDF2 expression was downregulated by the NF-κB, p38, and ERK inhibitors. YTHDF2 depletion increased the expression and stability of MAP2K4 and MAP4K4 mRNAs. All of these results suggest that YTHDF2 knockdown increases mRNA expression levels of MAP2K4 and MAP4K4 via stabilizing the mRNA transcripts, which activate MAPK and NF-κB signaling pathways, which promote the expression of proinflammatory cytokines and aggravate the inflammatory response in LPS-stimulated RAW 264.7 cells.

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“…LIG inhibited chondrocyte apoptosis and ameliorated cartilage degeneration via the JNK and p38 mitogen-activated protein kinas (MAPK) signalling pathways, leading to the down-regulation of inducible nitric oxide synthase (iNOS) and p-activating transcription factor 2 (ATF2) expression mitochondrial function deletion may be prior to the process of apoptosis. 35 Our data showed that LIG prevented the SNP-induced activation of JNK and p38 MAPK that consequently hindered the activation of ATF2 resulting in declined iNOS production. Our in vitro study confirmed that the overproduction of cleaved caspase-3, Bcl-2, Bax and iNOS after SNP stimulation was reversed by LIG at protein levels, and LIG exhibited anti-apoptotic and protective effects on 31 In addition, p38 MAPK is a vital signalling pathway that activates Bax subsequent to its translocation to the mitochondria.…”

Section: Discussionmentioning

confidence: 59%

“…34 JNK and p38 MAPK pathways trigger the transcription factor ATF2 that stimulates the iNOS promoter activity. 35 Our data showed that LIG prevented the SNP-induced activation of JNK and p38 MAPK that consequently hindered the activation of ATF2 resulting in declined iNOS production. Interestingly, the pretreatment with SP600125 or SB203580 significantly enhanced and anisomycin offset the LIG-induced effects, including the inhibition of ATF2, JNK and p38 MAPK phosphorylation, the down-regulation of iNOS release and cleaved caspase-3 activity, as well as the anti-apoptotic effect.…”

Section: Discussionmentioning

confidence: 59%

Ligustilide attenuates nitric oxide‐induced apoptosis in rat chondrocytes and cartilage degradation via inhibiting JNK and p38 MAPK pathways

Zhou

Jiang

et al. 2019

J Cellular Molecular Medi

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Ligustilide ( LIG ) is the main lipophilic component of the Umbelliferae family of pharmaceutical plants, including Radix angelicae sinensis and Ligusticum chuanxiong. LIG shows various pharmacological properties associated with anti‐inflammation and anti‐apoptosis in several kinds of cell lines. However, the therapeutic effects of LIG on chondrocyte apoptosis remain unknown. In this study, we investigated whether LIG had an anti‐apoptotic activity in sodium nitroprusside ( SNP )‐stimulated chondrocyte apoptosis and could delay cartilage degeneration in a surgically induced rat OA model, and elucidated the potential mechanisms. In vitro studies revealed that LIG significantly suppressed chondrocyte apoptosis and cytoskeletal remodelling, which maintained the nuclear morphology and increased the mitochondrial membrane potential. In terms of SNP , LIG treatment considerably reduced the expression levels of cleaved caspase‐3, Bax and inducible nitric oxide synthase and increased the expression level of Bcl‐2 in a dose‐dependent manner. The LIG ‐treated groups presented a significantly suppressed expression of activating transcription factor 2 and phosphorylation of Jun N‐terminal kinase ( JNK ) and p38 mitogen‐activated protein kinase ( MAPK ). The inhibitory effect of LIG was enhanced by the p38 MAPK inhibitor SB 203580 or the JNK inhibitor SP 600125 and offset by the agonist anisomycin. In vivo studies demonstrated that LIG attenuated osteoarthritic cartilage destruction by inhibiting the cartilage chondrocyte apoptosis and suppressing the phosphorylation levels of activating transcription factor 2, JNK and p38 MAPK . This result was confirmed by histological analyses, micro‐ CT , TUNEL assay and immunohistochemical analyses. Collectively, our studies indicated that LIG protected chondrocytes against SNP ‐induced apoptosis and delayed articular cartilage degeneration by suppressing JNK and p38 MAPK pathways.

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Wood-cultivated ginseng exerts anti-inflammatory effect in LPS-stimulated RAW264.7 cells

Cited by 26 publications

References 40 publications

Phenolic Compounds and Ginsenosides in Ginseng Shoots and Their Antioxidant and Anti-Inflammatory Capacities in LPS-Induced RAW264.7 Mouse Macrophages

Phenolic Compounds and Ginsenosides in Ginseng Shoots and Their Antioxidant and Anti-Inflammatory Capacities in LPS-Induced RAW264.7 Mouse Macrophages

m6A Reader YTHDF2 Regulates LPS-Induced Inflammatory Response

Ligustilide attenuates nitric oxide‐induced apoptosis in rat chondrocytes and cartilage degradation via inhibiting JNK and p38 MAPK pathways

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