The anti-inflammatory effect of <i>ent</i>-kaur-15-en-17-al-18-oic acid on lipopolysaccharide-stimulated RAW264.7 cells associated with NF-κB and P38/MAPK pathways

Zhang, Caiyun; Lin, Shiqi; Liu, Fang-Yuan; Ma, Jiahui; Jia, Fu-Juan; Han, Zhuo; Xie, Wenrui; Li, Xia

doi:10.1080/10286020.2020.1786371

Cited by 5 publications

(3 citation statements)

References 20 publications

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“…It has been widely known that nuclear factor-κB (NF-κB) is a typical pathway, which participates in inflammatory process via releasing excessive monocyte chemotactic protein-1 (MCP-1), nitric oxide (NO), inducible nitric oxide synthase (iNOS), and other inflammatory cytokines [24,25]. Mitogen-activated protein kinases (MAPKs) are critical to cell growth, differentiation, as well as proliferation, which are also responsible for the gene expression of inflammatory mediators [25]. Additionally, oxidative stress occurred when the steady-state of cellular redox is disrupted, which is always observed during the inflammatory response [26,27].…”

Section: Introductionmentioning

confidence: 99%

Comparation of Anti‐Inflammatory and Antioxidantactivities of Curcumin, Tetrahydrocurcuminand Octahydrocurcuminin LPS‐Stimulated RAW264.7 Macrophages

Xie

Cheng

Chen

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Curcumin (CUR) possesses pronounced anti-inflammatory and antioxidant activities. Generally, the clinical application of CUR is restricted due to its apparent unstability and poor absorption, and the biological activities of CUR may be closely associated with its metabolites. Tetrahydrocurcumin (THC) and octahydrocurcumin (OHC) are two major hydrogenated metabolites of CUR with appreciable biological potentials. Here, we comparatively explored the anti-inflammatory and antioxidant activities of CUR, THC, and OHC in lipopolysaccharide- (LPS-) induced RAW264.7 macrophages. The results revealed that CUR, THC, and OHC dose-dependently inhibited the generation of NO and MCP-1 as well as the gene expression of MCP-1 and iNOS. Additionally, CUR, THC, and OHC significantly inhibited NF-κB activation and p38MAPK and ERK phosphorylation, while substantially upregulated the Nrf2 target gene expression (HO-1, NQO-1, GCLC, and GCLM). Nevertheless, zinc protoporphyrin (ZnPP), a typical HO-1 inhibitor, significantly reversed the alleviative effect of CUR, THC, and OHC on LPS-stimulated ROS generation. These results demonstrated that CUR, THC, and OHC exerted beneficial effect on LPS-stimulated inflammatory and oxidative responses, at least partially, through inhibiting the NF-κB and MAPKs pathways and activating Nrf2-regulated antioxidant gene expression. Particularly, THC and OHC might exert superior antioxidant and anti-inflammatory activities to CUR in LPS-stimulated RAW264.7 cells, which can be further explored to be a promising novel effective agent for inflammatory treatment.

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Section: Introductionmentioning

confidence: 99%

Comparation of Anti‐Inflammatory and Antioxidantactivities of Curcumin, Tetrahydrocurcuminand Octahydrocurcuminin LPS‐Stimulated RAW264.7 Macrophages

Xie

Cheng

Chen

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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“…In this study, our findings revealed that OA, AA, and MA inhibited the nuclear translocation of NF-κB to different degrees and that OA had the strongest inhibitory effect. MAPK signaling pathway is involved in the inflammatory response [ 30 ]. We found that LPS-induced RAW264.7 cells increased the phosphorylation of P38, ERK1/2, and JNK1/2.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Activity of Three Triterpene from Hippophae rhamnoides L. in Lipopolysaccharide-Stimulated RAW264.7 Cells

Han

Yuan

Zhou

et al. 2021

IJMS

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Oleanolic acid (OA), asiatic acid (AA), and maslinic acid (MA) are ubiquitous isomeric triterpene phytochemicals with many pharmacological effects. To improve their application value, we used lipopolysaccharide (LPS) to induce RAW264.7 cells and studied the differences in the anti-inflammatory effects of the triterpenes according to their structural differences. MTT, Griess, and immunofluorescence assays, ELISA, flow cytometry, and Western blotting, were performed. The release of LPS-induced pro-inflammatory mediators, such as nitric oxide (NO), inducible nitric oxide synthase (iNOS), and interleukin (IL-6), was significantly inhibited by OA, AA, and MA at the same concentration, and AA and MA promoted the production of anti-inflammatory factor IL-10. OA, AA, and MA inhibited LPS-induced NF-κB nuclear translocation in RAW264.7 cells. OA and AA inhibited the phosphorylation of ERK1/2, P38, and JNK1/2 in LPS-stimulated RAW264.7 cells. Moreover, OA increased LPS-induced Nrf2 expression and decreased Keap1 expression in RAW264.7 cells. OA, AA, and MA inhibited LPS-stimulated intracellular reactive oxygen species (ROS) production and alleviated mitochondrial membrane potential depletion. Overall, our data suggested that OA, AA, and MA exhibited significant anti-inflammatory effects in vitro. In particular, OA and AA take effects through the MAPKs, NF-κB, and Nrf2 signaling pathways.

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“…Recent studies have demonstrated that the p38/MAPK signaling pathway is one of the most important signaling pathways, serving a critical role in the phosphorylation of substrates involved in the sepsis-induced inflammatory response ( 12 , 39 ). Certain studies have indicated that the p38/MAPK signaling pathway also serves an essential role in regulating oxidative stress-related signaling and participates in the pathogenesis of ALI ( 12 , 41 , 42 ). It is important to identify the changes in p38/MAPK activity associated with sepsis-induced ALI; therefore, the protein expression levels of p-p38 in the p38/MAPK signaling pathway were detected in the lung tissues of CLP-induced septic ALI model rats.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of taurine on sepsis‑induced lung injury via inhibiting the p38/MAPK signaling pathway

et al. 2021

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Sepsis, a leading cause of acute lung injury (ALI), is characterized by an overwhelming systemic inflammatory response and widespread organ injury, particularly in the lungs. Taurine, an intracellular free amino acid, has been used for the treatment of various diseases, including lung injury; however, the underlying mechanisms are unclear. The present study aimed to investigate the protective effect of taurine on septic ALI and the underlying mechanism. A septic ALI model was established by performing cecal ligation and puncture (CLP) surgery on Sprague Dawley rats. Following successful model establishment, rats were treated with taurine. The results of hematoxylin and eosin, respiratory function detection, malondialdehyde level and superoxide dismutase activity determination and ELSIA demonstrated that taurine significantly alleviated lung injury, restored respiratory function, reduced oxidation and decreased the concentrations of inflammatory factors in CLP-induced septic ALI model rats. In addition, compared with that in the ALI group, western blotting results indicated that taurine ameliorated lung epithelial injury by significantly increasing the expression levels of lung epithelial markers, E-cadherin and occludin. The western blotting results demonstrated that, compared with the control group, the p38/MAPK and NF-κB signaling pathways were significantly activated in CLP-induced septic ALI model rats, but taurine significantly suppressed ALI-mediated signaling pathway activation. To investigate the mechanism underlying taurine in the treatment of septic ALI, CLP-induced septic ALI model rats were treated with an antagonist of the p38/MAPK signaling pathway (SB203580). The effects of SB203580 on CLP-induced septic ALI model rats were similar to those of taurine. SB203580 significantly attenuated sepsis-induced lung injury and increases in IL-1β and TNF-α concentrations in the lung tissue. In addition, SB203580 promoted restoration of the injured lung tissue and respiratory function in CLP-induced septic ALI model rats. The western blotting results indicated that SB203580 significantly decreased the ratios of phosphorylated (p)-p38/p38 and p-p65/065, and increased the protein expression levels of E-cadherin and occludin compared with those in the ALI group. In summary, the present study demonstrated that taurine alleviated sepsis-induced lung injury, which was associated with suppression of the inflammatory response and oxidative stress via inhibiting the p38/MAPK signaling pathway. Therefore, the p38/MAPK signaling pathway may serve as a potential therapeutic target for the treatment of sepsis-induced ALI.

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The anti-inflammatory effect of ent-kaur-15-en-17-al-18-oic acid on lipopolysaccharide-stimulated RAW264.7 cells associated with NF-κB and P38/MAPK pathways

Cited by 5 publications

References 20 publications

Comparation of Anti‐Inflammatory and Antioxidantactivities of Curcumin, Tetrahydrocurcuminand Octahydrocurcuminin LPS‐Stimulated RAW264.7 Macrophages

Comparation of Anti‐Inflammatory and Antioxidantactivities of Curcumin, Tetrahydrocurcuminand Octahydrocurcuminin LPS‐Stimulated RAW264.7 Macrophages

Anti-Inflammatory Activity of Three Triterpene from Hippophae rhamnoides L. in Lipopolysaccharide-Stimulated RAW264.7 Cells

Protective effect of taurine on sepsis‑induced lung injury via inhibiting the p38/MAPK signaling pathway

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