Ginsenoside Rh2 Ameliorates Lipopolysaccharide Induced Acute Lung Injury by Regulating the TLR4/ PI3K/Akt/mTOR, Raf-1/MEK/ERK and Keap1/Nrf2/HO-1 Signaling Pathways in Mice

Hsieh, Ying‐Hen; Deng, Jeng-Shyan; Yuan-Shiun, Chang; Huang, Guan-Jhong

doi:10.20944/preprints201807.0426.v1

Cited by 30 publications

(26 citation statements)

References 3 publications

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“…In contrast, enhanced protein levels of NRF2 have been reported to alleviate LPS-induced lung injury in mice [39,40]. In consistent with previous report [41], we found that glycine pre-administration reversed LPS-induced depletion of NRF2 and led to the increased protein level of genes implicated in cellular survival [42]. In a recent study, the authors showed that NRF2 is a repressor of NF-κB [43].…”

Section: Discussionsupporting

confidence: 92%

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Zhang

Jiang

et al. 2020

Nutrients

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Glycine supplementation has been reported to alleviate lipopolysaccharide (LPS)-induced lung injury in mice. However, the underlying mechanisms responsible for this beneficial effect remain unknown. In the present study, male C57BL/6 mice were treated with aerosolized glycine (1000 mg in 5 mL of 0.9% saline) or vehicle (0.9% saline) once daily for 7 continuous days, and then were exposed to aerosolized LPS (5 mg in 5 mL of 0.9% saline) for 30 min to induce lung injury. Sera and lung tissues were collected 24 h post LPS challenge. Results showed that glycine pretreatment attenuated LPS-induced decreases of mucin at both protein and mRNA levels, reduced LPS-triggered upregulation of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interferons, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukins. Further study showed that glycine-reduced LPS challenge resulted in the upregulation of nuclear factor κB (NF-κB), nucleotide binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome. In addition, LPS exposure led to the downregulation of NRF2 and downstream targets, which were significantly improved by glycine administration in the lung tissues. Our findings indicated that glycine pretreatment prevented LPS-induced lung injury by regulating both NLRP3 inflammasome and NRF2 signaling.

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Section: Discussionsupporting

confidence: 92%

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Zhang

Jiang

et al. 2020

Nutrients

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“…Because exposure to IL-4, IL-10, or glucocorticoids could induce a type of M2-polarized macrophage [51,52], the previously reported induction of anti-inflammatory cytokine IL-10 by ginsenosides Rg6, Rb1, Rc, Rd, Re, Rf, Rg1, Rh1, Rh2, and Rp1, as well as compound K [14,23,24,41,[61][62][63][64][65][66][67], or activation of glucocorticoid receptors by compound K, ginsenosides Rg1, and Re [36][37][38][39] may imply that those ginsenosides could partly induce the resolution of inflammation through M2 polarization.…”

Section: Perspectivementioning

confidence: 99%

Pro-Resolving Effect of Ginsenosides as an Anti-Inflammatory Mechanism of Panax ginseng

2020

Biomolecules

129

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Panax ginseng, also known as Korean ginseng, is a famous medicinal plant used for the treatment of many inflammatory diseases. Ginsenosides (ginseng saponins) are the main class of active constituents of ginseng. The anti-inflammatory effects of ginseng extracts were proven with purified ginsenosides, such as ginsenosides Rb1, Rg1, Rg3, and Rh2, as well as compound K. The negative regulation of pro-inflammatory cytokine expressions (TNF-α, IL-1β, and IL-6) and enzyme expressions (iNOS and COX-2) was found as the anti-inflammatory mechanism of ginsenosides in M1-polarized macrophages and microglia. Recently, another action mechanism emerged explaining the anti-inflammatory effect of ginseng. This is a pro-resolution of inflammation derived by M2-polarized macrophages. Direct and indirect evidence supports how several ginsenosides (ginsenoside Rg3, Rb1, and Rg1) induce the M2 polarization of macrophages and microglia, and how these M2-polarized cells contribute to the suppression of inflammation progression and promotion of inflammation resolution. In this review, the new action mechanism of ginseng anti-inflammation is summarized.

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“…HO‐1 is a stress‐regulated protein induced by Nrf2 protects against the cytotoxicity of various oxidative stresses response. Nrf2 as a signaling protein can up‐regulate antioxidant enzymes, thereby reducing oxidative stress caused by ROS 11,34,35 . Moreover, previous study displayed that cisplatin damaged anti‐oxidant defense mechanisms followed by an apparent reduce in GSH and increase in MDA levels.…”

Section: Discussionmentioning

confidence: 98%

Protective effect of ginsenoside Rk1, a major rare saponin from black ginseng, on cisplatin‐induced nephrotoxicity in HEK‐293 cells

Jiang

et al. 2020

The Kaohsiung J of Med Scie

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Cisplatin, as one of the most effective chemotherapeutic agents, its clinical use is limited by serious side effect of nephrotoxicity. Cisplatin‐induced nephrotoxicity is closely related to apoptosis induction and activation of caspase. The present study aimed to explore the potential protective effect of ginsenoside Rk1 (Rk1), a rare ginsenoside generated during steaming ginseng, on cisplatin‐induced nephrotoxicity and the underlying mechanisms in human embryonic kidney 293 (HEK‐293) cells. Our results showed that the reduced cell viability induced by cisplatin could significantly recover by Rk1. Furthermore, glutathione (GSH) as an oxidative index, was elevated and the lipid peroxidation product malondialdehyde (MDA) was significantly decreased after Rk1 treatment compared to the cisplatin group. Additionally, Rk1 can also decrease the ROS fluorescence expression and increase the protein levels of nuclear factor erythroid 2‐related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) compared to the cisplatin group, which suggested a suppression of oxidative response. More importantly, the cisplatin‐induced elevated protein levels of Bax, cleaved caspase‐3, cleaved caspase‐9, and decreased protein level of Bcl‐2 were reversed after treatment with Rk1. Our results elucidated the possible protective mechanism of Rk1 for the first time, which may involve in its anti‐oxidation and anti‐apoptosis effects.

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Ginsenoside Rh2 Ameliorates Lipopolysaccharide Induced Acute Lung Injury by Regulating the TLR4/ PI3K/Akt/mTOR, Raf-1/MEK/ERK and Keap1/Nrf2/HO-1 Signaling Pathways in Mice

Cited by 30 publications

References 3 publications

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Glycine Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Regulating NLRP3 Inflammasome and NRF2 Signaling

Pro-Resolving Effect of Ginsenosides as an Anti-Inflammatory Mechanism of Panax ginseng

Protective effect of ginsenoside Rk1, a major rare saponin from black ginseng, on cisplatin‐induced nephrotoxicity in HEK‐293 cells

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