Ginsenoside Rb1 ameliorates Staphylococcus aureus-induced Acute Lung Injury through attenuating NF-κB and MAPK activation

Shaukat, Aftab; Guo, Yanxia; Jiang, Kangfeng; Zhao, Gan; Wu, Haichong; Zhang, Tao; Yang, Ye; Guo, Shanchun; Yang, Chao; Zahoor, Arshad; Akhtar, Muhammad Faheem; Umar, Talha; Shaukat, Irfan; Rajput, Shahid Ali; Hassan, Mubashar; Deng, Ganzhen

doi:10.1016/j.micpath.2019.05.003

Cited by 63 publications

(36 citation statements)

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“…Previous studies indicated that the NF‐κB signaling pathway is associated with cell proliferation and apoptosis. [ 32 ] To determine whether Rh2 induced apoptosis is related to the regulation of the NF‐κB signaling pathway in U20S cells, the expression of NF‐κB signaling pathway‐related protein was detected by Western blot analysis (Figure 8). The results proved that compared with the control group, the expression levels of phosphorylated p65 protein in the Rh2 group (8 and 80 μmol/L) were remarkably decreased in a concentration‐dependent manner.…”

Section: Resultsmentioning

confidence: 99%

Ginsenoside Rh2 impedes proliferation and migration and induces apoptosis by regulating NF‐κB, MAPK, and PI3K/Akt/mTOR signaling pathways in osteosarcoma cells

Gao

Feng

et al. 2020

J Biochem & Molecular Tox

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Ginsenoside Rh2 is a primary bioactive compound obtained from ginseng that indicated anticancer activities against several malignant tumors. However, previous studies have reported little about the inhibitory effect of Rh2 on osteosarcoma (OS). This study aims to explore whether Rh2 could exert anticancer effects in OS cells and further investigate the proliferation, migration, and apoptosis mechanisms induced by Rh2 in human OS U20S cell line. The viability of U20S cells was obtained by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay. Cell migration property was analyzed by wound-healing assay. Apoptosis was visualized using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL), 4′, 6-diamidino-2-phenylindole (DAPI), and annexin V/propidium iodide (PI) staining. Relative protein expressed was confirmed through Western blot analysis. Mitochondrial membrane potential was evaluated by JC-1 staining. In this study, we used broad-spectrum anticancer drug cisplatin (CP) as a positive control. The results indicated that Rh2 remarkably inhibited cell viability of U20S cells in a dose-and time-dependent manner, and suppressed migration. TUNEL, DAPI, annexin V/PI, and JC-1 assay suggested that Rh2 could induce cellular apoptosis. Rh2 could reduce the levels of Bcl-2, caspase 3, and caspase 9, and promote the expression level of Bax in U20S cells. Moreover, Rh2 could induce apoptosis by promoting mitogen-activated protein kinase (MAPK) signaling pathway and inhibit PI3K/Akt/mTOR and nuclear factor-κB (NF-κB) signaling pathway in U20S cells. These findings indicated that Rh2 has an anticancer effect on U20S cells by regulating MAPK, PI3K/Akt/mTOR, and NF-κB signaling pathway.

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Section: Resultsmentioning

confidence: 99%

Ginsenoside Rh2 impedes proliferation and migration and induces apoptosis by regulating NF‐κB, MAPK, and PI3K/Akt/mTOR signaling pathways in osteosarcoma cells

Gao

Feng

et al. 2020

J Biochem & Molecular Tox

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“…In the earliest stage of inflammation, IL-1β acts as a trigger for a subsequent cascade of inflammatory cytokines ( 35 ). IL-6 increases quickly in acute inflammation, which is often associated with injury, infections, and other stress ( 36 ). The adequate production of cytokines is very important for immune response and host defense.…”

Section: Discussionmentioning

confidence: 99%

Organic Selenium Ameliorates Staphylococcus aureus-Induced Mastitis in Rats by Inhibiting the Activation of NF-κB and MAPK Signaling Pathways

Liu

Ding

et al. 2020

Front. Vet. Sci.

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Mastitis is an economically important disease in dairy cows, which is often caused by Staphylococcus aureus ( S. aureus ). Selenium is an indispensable element for physiological function and contributes to reduce injury of the mammary glands in mastitis. However, adequate sources of selenium have always been an important consideration for livestock. Therefore, the study aimed to explore the protective effect and mechanism of Selenohomolanthionine (SeHLan) on mastitis induced by S. aureus . The S. aureus -induced rat model was established and three doses (0.2, 2, 20 μg/kg body weight/day) of dietary OS were supplemented. The bacterial load, histopathology, and myeloperoxidase (MPO) of the mammary glands were performed and determined. Cytokines, including interleukin (IL)-1β, TNF-α, and IL-6, were detected using qRT-PCR. The key proteins of NF-κB and MAPK signaling pathways were analyzed by Western blot. The results revealed that OS supplementation could reduce the recruitment of neutrophils and macrophages in mammary tissues, but did not decrease S. aureus load in the tissues. The overexpression levels of IL-1β, TNF-α, and IL-6 induced by S. aureus were inhibited after OS treatment. Furthermore, the increased phosphorylation of NF-κB and MAPKs proteins were also suppressed. The results suggest that dietary supplementation with adequate OS during pregnancy contributes to protect the mammary glands from injury caused by S. aureus and alleviate the inflammatory response.

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“…Furthermore, GRg3 can inhibit P-glycoprotein expression and increase the accumulation of drugs such as vincristine in multidrug resistant cells, but not in sensitive cells (Kim et al, 2003). Importantly, it has been reported that some ginsenosides can inhibit the activation of IRAK1 and its downstream pathways (Joh et al, 2011;Nag et al, 2012;Shaukat et al, 2019). In this study, we investigated the in vitro anti-viability of ginsenoside panaxatriol (GPT) in TNBC PTX resistant cells, and found that GPT can target IRAK1/NF-κB and ERK pathways to overcome resistance.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside panaxatriol reverses TNBC paclitaxel resistance by inhibiting the IRAK1/NF-κB and ERK pathways

Wang

Song

Wan

et al. 2020

PeerJ

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Background Paclitaxel (PTX) resistance is a major obstacle in the treatment of triple-negative breast cancer (TNBC). Previously, we have reported that interleukin-1 receptor-associated kinase 1 (IRAK1) and its downstream pathways are associated with PTX resistance in TNBC cells. In this study, we sought to investigate the combination treatment of ginsenoside panaxatriol (GPT), one of the main active components in Panax ginseng, with PTX on viability and apoptosis of TNBC PTX resistant cells, and explore the role of IRAK1 mediated signaling pathways in the therapeutic effects. Methods CellTiter-Glo and colony formation assays were used to assess cell viability. Flow cytometry was used to analyze subG1 and apoptosis. Western blot was used to detect expressions of proteins involved in apoptosis and the IRAK1/NF-κB and ERK pathways. The mRNA expression of inflammatory cytokines, S100A7/8/9 and cancer stem cell (CSC)-related genes were examined by qPCR. Stem cells were identified by tumor sphere assay. Cell invasion ability was examined by transwell assay. Results We show that GPT inhibits MDA-MB-231 PTX resistant (MB231-PR) cell viability in a dose-dependent manner. When combined with PTX, GPT synergistically causes more cell death, induces subG1 accumulation and cell apoptosis. Besides, up-regulation of BAX/BCL-2 ratio, and down-regulation of MCL-1 are also observed. Moreover, this combination inhibits IRAK1, NF-κB and ERK1/2 activation, and leads to down-regulation of inflammatory cytokines (IL6, IL8, CXCL1, CCL2), S100A7/9 and CSC-related genes (OCT4, SOX2, NANOG, ALDH1, CD44) expression. In addition, the combination treatment suppresses MB231-PR cell invasion ability, and impairs tumor sphere growth both in MB231-PR and SUM159 PTX resistant (SUM159-PR) cells. Conclusion Our study demonstrates that GPT can resensitize TNBC PTX resistant cells to PTX by inhibiting the IRAK1/NF-κB and ERK pathways and reducing stem cell characteristics.

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Ginsenoside Rb1 ameliorates Staphylococcus aureus-induced Acute Lung Injury through attenuating NF-κB and MAPK activation

Cited by 63 publications

References 36 publications

Ginsenoside Rh2 impedes proliferation and migration and induces apoptosis by regulating NF‐κB, MAPK, and PI3K/Akt/mTOR signaling pathways in osteosarcoma cells

Ginsenoside Rh2 impedes proliferation and migration and induces apoptosis by regulating NF‐κB, MAPK, and PI3K/Akt/mTOR signaling pathways in osteosarcoma cells

Organic Selenium Ameliorates Staphylococcus aureus-Induced Mastitis in Rats by Inhibiting the Activation of NF-κB and MAPK Signaling Pathways

Ginsenoside panaxatriol reverses TNBC paclitaxel resistance by inhibiting the IRAK1/NF-κB and ERK pathways

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