Ruscogenin alleviates LPS-induced pulmonary endothelial cell apoptosis by suppressing TLR4 signaling

Wu, Yunhao; Wang, Yuwei; Gong, Shuaishuai; Tang, Jiahui; Zhang, Jiazhi; Li, Fang; Yu, Boyang; Zhang, Yuanyuan; Kou, Junping

doi:10.1016/j.biopha.2020.109868

Cited by 40 publications

(33 citation statements)

References 39 publications

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“…The results confirm that PA decreases HUVECs viability and promotes their apoptosis. Ruscogenin has been shown to reduce lipopolysaccharide-induced endothelial cell apoptosis [14]. The present findings demonstrated that ruscogenin exerted an anti-cytotoxic effect in PA-induced HUVECs as evidenced by decreased apoptosis and increased cell viability.…”

Section: Discussionsupporting

confidence: 64%

Ruscogenin alleviates palmitic acid-induced endothelial cell inflammation by suppressing TXNIP/NLRP3 pathway

Liu¹,

Zheng²,

Xiong³

et al. 2020

Trop. J. Pharm Res

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Purpose: To investigate the involvement of ruscogenin in palmitic acid (PA)-induced endothelial cell inflammation. Method: Cultured human umbilical vein endothelial cells (HUVECs) were divided into five groups: control (normal untreated cells), PA (cell treated with palmitic acid), and PA + ruscogenin (1, 10, or 30 μM). Cell viability and apoptosis rate were determined using MTT (3-(4,5)-dimethylthiahiazo(-z-y1)-3,5- di-phenytetrazolium bromide) and flow cytometry assays, respectively. The levels of cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemo-attractant protein-1 (MCP-1) were determined by an enzyme-linked immunosorbent assay. Western blotting and real-time polymerase chain reaction (RT-PCR) were used to evaluate the underlying mechanisms of action. Results: PA treatment decreased the viability of HUVECs and induced apoptosis (p < 0.05). Ruscogenin attenuated PA-induced cell death in a dose-dependent manner (p < 0.05). On the other hand, PA induced an increase in IL-1β, TNF-α, ICAM-1, MCP-1, TXNIP (thioredoxin-interacting protein),as well as NLRP3 (nucleotide oligomerization domain-, leucine-rich repeat- and pyrin domain-containing protein 3), all of which were attenuated by ruscogenin (p < 0.05). Conclusion: Ruscogenin alleviates PA-induced endothelial cell inflammation via TXNIP/NLRP3 pathway, thereby providing an insight into new therapeutic strategies to treat cardiovascular diseases. Keywords: Ruscogenin, Palmitic acid, Endothelial cells, Inflammation, TXNIP, NLRP3, Cardiovascular diseases

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Section: Discussionsupporting

confidence: 64%

Ruscogenin alleviates palmitic acid-induced endothelial cell inflammation by suppressing TXNIP/NLRP3 pathway

Liu¹,

Zheng²,

Xiong³

et al. 2020

Trop. J. Pharm Res

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“…Studies have shown that LPS promotes the excessive production of in ammatory mediators by activating the TLR4/Myd88 signaling pathway, leading to lung damage and ALI progression [27,28]. Recent studies have shown that several natural products modulate the in ammatory response by inhibiting the TLR4/NF-κB signaling pathway [29][30][31][32][33]. Our results showed that astaxanthin inhibit the TLR4/MyD88/NF-κB signaling pathway.…”

Section: Discussionsupporting

confidence: 59%

Exploring the mechanism of astaxanthin against lipopolysaccharide-induced acute lung injury by network pharmacology and experimental validation

Luo

Huang

et al. 2021

Preprint

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BackgroundAcute lung injury (ALI) is a leading cause of morbidity and mortality in respiratory disease. Astaxanthin, a natural antioxidant xanthophyll carotenoid, has been shown to possess anti-inflammatory activity. However, poor evidence has been reported that whether it has protective effects against ALI.Methods A network pharmacology analysis was carried out combining the construction of the GeneCards database and the Pharmmapper database, The potential active compounds and targets were predicted by compound-target prediction, protein-protein interaction analysis, GO and KEGG pathway analysis. Then, the anti-inflammation effect of astaxanthin was investigated in LPS-induced RAW264.7 cells in vitro and LPS-induced ALI mice in vivo.ResultsThe results screened by GO and KEGG enrichment analysis suggested that astaxanthin had extensive associations with 25 known therapeutic targets of ALI. These target genes were further found to be associated with pathways involved in inflammatory pathways in ALI, such as the Toll-like receptor signal pathway, TNF signal pathway, Hif signal pathway, and NF-Kappa B signal pathway. Pre-treatment with astaxanthin inhibited the TLR4/MyD88 signaling pathway and attenuated LPS-increased inflammatory factors in vitro. Furthermore, the administration of astaxanthin significantly protected lung injury in vivo. Subsequently, we validated astaxanthin binds to the TLR4 pocket using molecular docking. ConclusionTaken together, astaxanthin exerts impressively protective effects on LPS-induced ALI in vitro and in vivo via suppressing the TLR4/MyD88 signaling pathway.

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“…In addition, ruscogenin also prevented apoptosis of pulmonary endothelial cells. The TLR4/MYD88/NF-κB and Bax/Bcl-2 signaling pathways were involved in the process [ 399 , 400 ].…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

Zhou

et al. 2021

Pharmacological Research

216

121

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Ruscogenin alleviates LPS-induced pulmonary endothelial cell apoptosis by suppressing TLR4 signaling

Cited by 40 publications

References 39 publications

Ruscogenin alleviates palmitic acid-induced endothelial cell inflammation by suppressing TXNIP/NLRP3 pathway

Ruscogenin alleviates palmitic acid-induced endothelial cell inflammation by suppressing TXNIP/NLRP3 pathway

Exploring the mechanism of astaxanthin against lipopolysaccharide-induced acute lung injury by network pharmacology and experimental validation

Natural product derived phytochemicals in managing acute lung injury by multiple mechanisms

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