Rotundic acid reduces <scp>LPS</scp>‐induced acute lung injury in vitro and in vivo through regulating <scp>TLR4</scp> dimer

Li, Xinxing; Yuan, Renyikun; Wang, Qinqin; Han, Shan; Liu, Zhenjie; Xu, Qiong; Yang, Shilin

doi:10.1002/ptr.7152

Cited by 12 publications

(8 citation statements)

References 58 publications

(73 reference statements)

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“…However, HSC effectively inhibits this NF‐kB/p65 nuclear translocation, as confirmed by immunofluorescence data (Figure 3h,i). The activation of the NF‐κB signaling pathway leads to the production of pro‐inflammatory factors like TNF‐α and IL‐6 (Li, Yuan, et al, 2021). RT‐qPCR, as shown in Figure 3f,g, was used to study the impact of HSC on the release of TNF‐α and IL‐6.…”

Section: Resultsmentioning

confidence: 99%

“…This action triggers the discharge of calcium ions from internal storage or stimulates PKC to control subsequent signaling processes (Suh et al, 2008). The activation of the NF-κB signaling pathway leads to the production of pro-inflammatory factors like TNF-α and IL-6 (Li, Yuan, et al, 2021). RT-qPCR, as shown in Figure 3f,g, was used to study the impact of HSC on the release of TNF-α and IL-6.…”

Section: Hsc Suppresses Nlrp3 Inflammasome Activation In Lps + Atp-in...mentioning

confidence: 99%

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Hederasaponin C inhibits LPS‐induced acute kidney injury in mice by targeting TLR4 and regulating the PIP2/NF‐κB/NLRP3 signaling pathway

Han,

Li,

et al. 2023

Phytotherapy Research

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Acute kidney injury (AKI) is a common clinical condition associated with increased incidence and mortality rates. Hederasaponin C (HSC) is one of the main active components of Pulsatilla chinensis (Bunge) Regel. HSC possesses various pharmacological activities, including anti‐inflammatory activity. However, the protective effect of HSC against lipopolysaccharide (LPS)‐induced AKI in mice remains unclear. Therefore, we investigated the protective effect of HSC against LPS‐induced renal inflammation and the underlying molecular mechanisms. Herein, using MTT and LDH assays to assess both cell viability and LDH activity; using dual staining techniques to identify different cell death patterns; conducting immunoblotting, QRT‐PCR, and immunofluorescence analyses to evaluate levels of protein and mRNA expression; employing immunoblotting, molecular docking, SPR experiments, and CETSA to investigate the interaction between HSC and TLR4; and studying the anti‐inflammatory effects of HSC in the LPS‐induced AKI. The results indicate that HSC inhibits the expression of TLR4 and the activation of NF‐κB and PIP2 signaling pathways, while simultaneously suppressing the activation of the NLRP3 inflammasome. In animal models, HSC ameliorated LPS‐induced AKI and diminished inflammatory response and the level of renal injury markers. These findings suggest that HSC has potential as a therapeutic agent to mitigate sepsis‐related AKI.

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Section: Resultsmentioning

confidence: 99%

Section: Hsc Suppresses Nlrp3 Inflammasome Activation In Lps + Atp-in...mentioning

confidence: 99%

Hederasaponin C inhibits LPS‐induced acute kidney injury in mice by targeting TLR4 and regulating the PIP2/NF‐κB/NLRP3 signaling pathway

Han,

Li,

et al. 2023

Phytotherapy Research

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“…A recent study has shown that CYR61 can promote the expression of TLR4, 31 while TLR4 is widely involved in promoting acute lung injury. [32][33][34] The stated study indicated that TLR4/MYD88 signaling pathway was activated by induction of LPS, which was suppressed by the interference of KLF6. Consistent with the previous study, 31 overexpression of CYR61 promoted the expressions of TLR4 and MYD88 in LPS-induced A549 cells transfected with Si-KLF6.…”

Section: Cyr61 Overexpression Reversed the Inhibitory Effect Of Inter...mentioning

confidence: 94%

Inhibition of KLF6 reduces the inflammation and apoptosis of type II alveolar epithelial cells in acute lung injury

Chen

Jia

2022

Allergol Immunopathol

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Background: The development of acute lung injury (ALI) into a severe stage leads to acute respi-ratory distress syndrome (ARDS). The morbidity and mortality of ALI and ARDS are very high. Objective: This study is aimed to explore the effect of Krüppel-like factor 6 (KLF6) on lipopoly-saccharide (LPS)-induced type II alveolar epithelial cells in ALI by interacting with cysteine-rich angiogenic inducer 61 (CYR61). Material and Methods: ALI mice model and LPS-induced type II alveolar epithelial cells were conducted to simulate ALI in vivo and in vitro. The messenger RNA (mRNA) and protein expres-sion of KLF6 in lung tissues were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis. Pathological changes in lung tissues were observed by hematoxylin and eosin (H&E) staining. The viability and KLF6 expression of A549 cells treated with different concentrations of LPS were detected by cell counting kit-8 (CCK-8) assay, RT-qPCR, and Western blot analysis. After indicated treatment, the viability and apoptosis of A549 cells were analyzed by CCK-8 and TUNEL assays, and the inflammation factors of A549 cells were detected by Enzyme-linked-immunosorbent serologic assay, RT-qPCR, and Western blot analysis. The combination of KLF6 and CYR61 was determined by chromatin immunoprecipitation (ChIP)-PCR and dual-luciferase reporter assay. Results: KLF6 expression was increased in lung tissues of ALI mice and LPS-induced A549 cells. Interference with KLF6 improved the viability, reduced the inflammatory damage, and promoted the apoptosis of LPS-induced A549 cells. In addition, KLF6 could bind to CYR61. Interference with KLF6 could decrease CYR61 expression in LPS-induced A549 cells. LPS also enhanced the TLR4/MYD88 signaling pathway, which was reversed by KLF6 interference. The above phenomena in LPS-induced A549 cells transfected with Si-KLF6 could be reversed by overexpression of CYR61. Conclusion: Inhibition of KLF6 promoted the viability and reduced the inflammation and apop-tosis of LPS-induced A549 cells, which was reversed by CYR61.

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“…The study also revealed that RA obstructed the activation of the PI3K, MAPK, and NF-kB pathways while enhancing the activity of the Nrf2 signaling pathway. [80] The antioxidant and anti-inflammatory effects of RA and their molecular mechanisms are clarified in Table 2.…”

Section: Anti-inflammatory Activitymentioning

confidence: 99%

Efficacy of Rotundic Acid and Its Derivatives as Promising Natural Anticancer Triterpenoids: A Literature‐Based Study

Bhuia,

Chowdhury,

Sonia

et al. 2024

Chemistry & Biodiversity

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Rotundic acid (RA) is a naturally occurring pentacyclic triterpene with a multitude of pharmacological activities. The primary emphasis of this study is on summarizing the anticancer properties with the underlying mechanisms of RA and its derivatives, as well as the pharmacokinetic features. Data was collected (up to date as of November 10, 2023) from various reliable and authentic literatures by searching in different academic search engines, including PubMed, Springer Link, Scopus, Wiley Online, Web of Science, ScienceDirect, and Google Scholar. The findings imply that RA and its synthetic derivatives possess promising anti‐cancer properties against breast, colorectal, liver, and cervical cancers in various preclinical pharmacological test systems. The results also indicate that RA and its derivatives demonstrated anticancer effects via a number of cellular mechanisms, including apoptotic cell death, inhibition of oxidative stress, anti‐inflammatory effect, cytotoxicity, cell cycle arrest, anti‐proliferative effect, anti‐angiogenic effect, and inhibition of cancer cell migration and invasion. It has been proposed that RA and its derived compounds have the capability to serve as a hopeful chemotherapeutic agent, so further extensive clinical research is necessary.

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Rotundic acid reduces LPS‐induced acute lung injury in vitro and in vivo through regulating TLR4 dimer

Cited by 12 publications

References 58 publications

Hederasaponin C inhibits LPS‐induced acute kidney injury in mice by targeting TLR4 and regulating the PIP2/NF‐κB/NLRP3 signaling pathway

Hederasaponin C inhibits LPS‐induced acute kidney injury in mice by targeting TLR4 and regulating the PIP2/NF‐κB/NLRP3 signaling pathway

Inhibition of KLF6 reduces the inflammation and apoptosis of type II alveolar epithelial cells in acute lung injury

Efficacy of Rotundic Acid and Its Derivatives as Promising Natural Anticancer Triterpenoids: A Literature‐Based Study

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