Paeonol Inhibits IL-1β-Induced Inflammation via PI3K/Akt/NF-κB Pathways: In Vivo and Vitro Studies

Lou, Yiting; Wang, Chenggui; Tang, Qian; Zheng, Wenhao; Feng, Zhenhua; Yu, Xingfang; Guo, Xiaoshan; Wang, Jianshun

doi:10.1007/s10753-017-0611-8

Cited by 62 publications

(43 citation statements)

References 22 publications

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“…In harmony with the present study, several previous studies [47,48] noted similar findings regarding the ability of paeonol to decrease the NO level. NO, a short-lived gasotransmitter, is known as a mediator and regulator of inflammatory responses.…”

Section: Discussionsupporting

confidence: 93%

Paeonol Attenuates Methotrexate-Induced Cardiac Toxicity in Rats by Inhibiting Oxidative Stress and Suppressing TLR4-Induced NF-κB Inflammatory Pathway

Al‐Taher

Morsy

Rifaai

et al. 2020

Mediators of Inflammation

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Methotrexate (MTX) is a commonly used chemotherapeutic agent. Oxidative stress and inflammation have been proved in the development of MTX toxicity. Paeonol is a natural phenolic compound with various pharmacological activities including antioxidant and anti-inflammatory properties. The aim of the present study was to evaluate the protective effect of paeonol against MTX-induced cardiac toxicity in rats and to evaluate the various mechanisms that underlie this effect. Paeonol (100 mg/kg) was administered orally for 10 days. MTX cardiac toxicity was induced at the end of the fifth day of the experiment, with or without paeonol pretreatment. MTX-induced cardiac damage is evidenced by a distortion in the normal cardiac histological structure, with significant oxidative and nitrosative stress shown as a significant increase in NADPH oxidase-2, malondialdehyde, and nitric oxide levels along with a decrease in reduced glutathione concentration and superoxide dismutase activity compared to the control group. MTX-induced inflammatory effects are evidenced by the increased cardiac toll-like receptor 4 (TLR4) mRNA expression and protein level as well as increased cardiac tumor necrosis factor- (TNF-) α and interleukin- (IL-) 6 levels along with increased nuclear factor- (NF-) κB/p65 immunostaining. MTX increased apoptosis as shown by the upregulation of cardiac caspase 3 immunostaining. Paeonol was able to correct the oxidative and nitrosative stress as well as the inflammatory and apoptotic parameters and restore the normal histological structure compared to MTX alone. In conclusion, paeonol has a protective effect against MTX-induced cardiac toxicity through inhibiting oxidative and nitrosative stress and suppressing the TLR4/NF-κB/TNF-α/IL-6 inflammatory pathway, as well as causing an associated reduction in the proapoptotic marker, caspase 3.

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Section: Discussionsupporting

confidence: 93%

Paeonol Attenuates Methotrexate-Induced Cardiac Toxicity in Rats by Inhibiting Oxidative Stress and Suppressing TLR4-Induced NF-κB Inflammatory Pathway

Al‐Taher

Morsy

Rifaai

et al. 2020

Mediators of Inflammation

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“…study demonstrating the ability of paeonol to inhibit expression of MMPs and loss of type II collagen in rabbit chondrocytes. Also in accordance with the findings of the same study, we reveal that paeonol treatment inhibited activation of NF-jB [39]. Activation of NF-jB triggered by IjBa phosphorylation and subsequent nuclear translocation of p65 governs the expression of a massive array of inflammatory processes.…”

Section: Discussionsupporting

confidence: 92%

Paeonol prevents IL-1β-induced inflammatory response and degradation of type II collagen in human primary chondrocytes

Wang¹,

Kang³

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Li (2019) Paeonol prevents IL-1β-induced inflammatory response and degradation of type II collagen in human primary chondrocytes, Artificial ABSTRACT Osteoarthritis (OA) is a common joint disease for which a safe and reliable treatment has yet to be developed. Here, we demonstrated the potential benefit of treatment with paeonol, a derivative of Paeonia suffruticosa, in the treatment and prevention of OA. Chondrogenic cell line ATDC5 cells were cultured with IL-1b and the effects of paeonol were assessed through qRT-PCR, western blot analysis, MTT, ELISA, and NF-jB luciferase reporter gene assay. Our findings demonstrate a novel ability of paeonol to inhibit numerous factors of OA, including expressions of IL-6, TNF-a, NOX2, PTGS2, NUCB2/nesfatin-1, ICAM-1, VCAM-1, MMP-3/13, degradation of type II collagen, and NF-jB activation through the rescue of IjBa. Additionally, we assessed the effects of paeonol on cell viability to confirm its safety. These findings implicate a valuable potential role of paeonol in the treatment and prevention of OA. ARTICLE HISTORY

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“…The activation of the PI3K/Akt pathway can result in diverse regulations due to its broad range of target proteins such as mTOR, NF-κB, GSK-3β, and p53 64 . Nevertheless, PI3K/Akt has been reported to be involved in OA regulation and progression since its overactivation leads to inflammation and apoptosis of chondrocytes 65 , 66 . Activation of Akt and thereby induced apoptosis could be linked to the observed reduced pellet size and DNA content in HP-stimulated group compared to unstimulated samples (Figs 4 and 5 , Supplementary Fig.…”

Section: Discussionmentioning

confidence: 99%

Hydrostatic pressure-generated reactive oxygen species induce osteoarthritic conditions in cartilage pellet cultures

Rieder

Weihs

Weidinger

et al. 2018

Sci Rep

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Osteoarthritis (OA) is one of the most common causes of disability and represents a major socio-economic burden. Despite intensive research, the molecular mechanisms responsible for the initiation and progression of OA remain inconclusive. In recent years experimental findings revealed elevated levels of reactive oxygen species (ROS) as a major factor contributing to the onset and progression of OA. Hence, we designed a hydrostatic pressure bioreactor system that is capable of stimulating cartilage cell cultures with elevated ROS levels. Increased ROS levels in the media did not only lead to an inhibition of glycosaminoglycans and collagen II formation but also to a reduction of already formed glycosaminoglycans and collagen II in chondrogenic mesenchymal stem cell pellet cultures. These effects were associated with the elevated activity of matrix metalloproteinases as well as the increased expression of several inflammatory cytokines. ROS activated different signaling pathways including PI3K/Akt and MAPK/ERK which are known to be involved in OA initiation and progression. Utilizing the presented bioreactor system, an OA in vitro model based on the generation of ROS was developed that enables the further investigation of ROS effects on cartilage degradation but can also be used as a versatile tool for anti-oxidative drug testing.

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Paeonol Inhibits IL-1β-Induced Inflammation via PI3K/Akt/NF-κB Pathways: In Vivo and Vitro Studies

Cited by 62 publications

References 22 publications

Paeonol Attenuates Methotrexate-Induced Cardiac Toxicity in Rats by Inhibiting Oxidative Stress and Suppressing TLR4-Induced NF-κB Inflammatory Pathway

Paeonol Attenuates Methotrexate-Induced Cardiac Toxicity in Rats by Inhibiting Oxidative Stress and Suppressing TLR4-Induced NF-κB Inflammatory Pathway

Paeonol prevents IL-1β-induced inflammatory response and degradation of type II collagen in human primary chondrocytes

Hydrostatic pressure-generated reactive oxygen species induce osteoarthritic conditions in cartilage pellet cultures

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