Paeonol attenuates acute lung injury by inhibiting HMGB1 in lipopolysaccharide-induced shock rats

Liu, Xia; Xu, Qin; Mei, Liyan; Lei, Hang; Wen, Quan; Miao, Jifei; Huang, Haoming; Chen, Dongfeng; Du, Shisuo; Zhang, Saixia; Zhou, Jianhong; Deng, Ran; Li, Yiwei; Li, Chun; Li, Hui

doi:10.1016/j.intimp.2018.05.032

Cited by 29 publications

(25 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… Compounds Structure In vitro/in vivo Model (effective dose) Cells (effective concentration) Related pharmacological indicators Related molecular mechanisms Refs. Honokiol 91 CLP/LPS (5 mg/kg) HPMECs (5 μM) MPO↓ TNF-α↓ IL-6↓ MDA↓ iNOS↓ ICAM-1↓ NO↓ HMGB1↓ Activation of Sirt3/AMPK signaling axis [ [283] , [284] , [285] ] Paeonol 92 LPS (0.146 mg/kg) MPO↓ TNF-α↓ IL-1β↓ IL-6↓ HMGB1↓ Inhibition of HMGB1 and TLR4/MyD88/NF-κB signaling pathway [ 286 , 287 ] Magnolol 93 LPS (10 mg/kg) MPO↓ TNF-α↓ IL-1β↓ IL-6↓ COX-2↓ iNOS↓ Activation of PPAR-γ Inhibition of TLR4 mediated NF-kB signaling pathway [ [288] , [289] , [290] , [291] ] Curcumin 94 Bleomycin/LPS/CLP/Lethal gramnegative (150 mg/kg) TNF-α↓ IL-1β↓ IL-6↓ TGF-β↓ HMGB1↓ IL-17A↓ IL-10↑ Inhibition of IL-17A mediated p53-fibrinolytic system, PPARγ/HO1 regulated-HMGB1/RAGE, MAPK signaling pathway, TGF-β1/SMAD3 signaling pathway and NF-κB pathways [ [292] , [293] , [294] , [295] , [296] , [297] , [298] ] Zingerone 95 LPS (20 mg/kg) RAW 264.7 (12.5 μg/mL) MPO↓ TNF-α↓ IL-1β↓ IL-6↓ Inhibition of NF-κB and MAPK signaling pathways [ 299 ] Octyl gallate 96 ...…”

Section: Mechanisms Involved In Ali/ardsmentioning

confidence: 99%

“…et Wils. It significantly improved animal survival rate and mean arterial pressure, attenuated lung pathological damage as well as reduced inflammatory cytokine expression (TNF-α, IL-1β and IL-6) through regulating the TLR4/MyD88/NF-κB [ 286 ] and HMGB1 signaling pathways in a LPS-induced ALI model [ 287 ].…”

Section: Natural Compounds That Exert Anti-ali Effectsmentioning

confidence: 99%

See 1 more Smart Citation

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

Zhou

et al. 2021

Pharmacological Research

216

121

View full text Add to dashboard Cite

show abstract

Section: Mechanisms Involved In Ali/ardsmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…Following the synthesis and release of HMGB1, pro-inflammatory factors, such as TNF-α and IL-1 further promote mononuclear/macrophages, endothelial cells, neuronal cells, NK cells, and other cells to actively secrete HMGB1; thus, forming a positive feedback loop. This leads to the continuous promotion of the inflammatory response [6,8,9].…”

mentioning

confidence: 99%

Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury

et al. 2020

View full text Add to dashboard Cite

Background: Kawasaki disease (KD) is a common, yet unknown etiology disease in Asian countries, which causes acquired heart disease in childhood. It is characterized by an inflammatory acute febrile vasculitis of medium-sized arteries, particularly the coronary arteries. High-mobility group box-1 protein (HMGB1) is a non-histone chromosomalbinding protein present in the nucleus of eukaryotic cells, which contains 215 amino acid residues. Although the cellular signal transduction mechanisms of HMGB1 are currently unclear, the important role of the receptor for advanced glycation end-products (RAGE), the main receptor for HMGB1 has been reported in detail. The purpose of our study was to verify the mechanism and clinical significance of HMGB1-RAGE in coronary artery injury of Kawasaki disease. Methods: 52 blood samples of patients in KD were collected, and the coronary artery Z score was calculated according to the echocardiographic results. The Z score ≥ 2.0 was classified as coronary artery lesions (CAL); otherwise, it was no-coronary artery lesions (NCAL). In addition, the fever group and control group were set. Among them, the fever group were children with fever due to respiratory tract infection at the same time period as KD (heat peak ≥ 38.5 ℃). The normal group were children at a routine physical examination in the outpatient clinic of Nantong University and the physical examination center of the child care insurance, and there were no infectious diseases and heart diseases. The serum levels of HMGB1, RAGE, and NF-κB in each group were detected by ELISA. The animal model of KD was established using the New Zealand young rabbits. We used RT-qPCR/H&E staining/immunohistochemistry/ELISA and western blot to detect the level of HMGB1/RAGE and NF-κB. Results: In this study, we found that the HMGB1/RAGE/NF-κB axis was elevated in the serum of children with KD. In addition, an animal model of KD was subsequently prepared to examine the pathological changes of the coronary arteries. We found that the serum levels of HMGB1/RAGE/NF-κB in rabbits with KD were significantly higher than those of the control group. Moreover, the lumen diameter of the coronary artery was slightly enlarged, and the wall of the tube became thinner and deformed. In addition, the HMGB1/RAGE/NF-κB levels in the coronary artery were higher in the rabbits with KD in the acute phase. Conclusions: On the whole, the findings of this study demonstrate that the expression of HMGB1/RAGE/NF-κB is altered at different stages of KD, suggesting that the HMGB1/RAGE/NF-κB signaling pathway plays an important role in vascular injury in KD. The results of this study may have important implications for the early warning of coronary artery lesions in KD.

show abstract

“…Chronic inflammation plays a major role in various chronic diseases, such as respiratory, cardiovascular, gastrointestinal, hepatobiliary, urogenital, neurological, skeletal, rheumatological systems, and cancer diseases [43][44][45][46][47][48]. e effect of Cynanchum paniculatum and its derivatives on [31,[49][50][51][52]. e mechanism of action mostly involves the inhibition of TLR4/NF-κB and MAPK signaling and the inhibition of ROS-sensitive inflammatory signaling [31,32].…”

Section: Modulation Of Inflammation By Cynanchum Paniculatum and Its mentioning

confidence: 99%

“…The elevation of inflammatory mediators, such as TNF- α , IL-1 β , reactive oxygen species (ROS), and NO, can be cardiodepressive and can contribute to multiorgan dysfunction syndrome with disease progression. Recently, increasing research attention and research outcomes have suggested the role of Cynanchum paniculatum and paeonol in pulmonary diseases, including asthma, airway inflammation, cigarette smoke-induced pulmonary inflammation, and fibrosis [ 31 , 49 – 52 ]. The mechanism of action mostly involves the inhibition of TLR4/NF- κ B and MAPK signaling and the inhibition of ROS-sensitive inflammatory signaling [ 31 , 32 ].…”

Section: Modulation Of Inflammation By Cynanchum Paniculmentioning

confidence: 99%

Cynanchum paniculatum and Its Major Active Constituents for Inflammatory‐Related Diseases: A Review of Traditional Use, Multiple Pathway Modulations, and Clinical Applications

Chen

Cheng

Chen

et al. 2020

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Cynanchum paniculatum Radix, known as Xuchangqing in Chinese, is commonly prescribed in Chinese Medicine (CM) for the treatment of various inflammatory diseases. The anti-inflammatory property of Cynanchum paniculatum can be traced from its wind-damp removing, collaterals’ obstruction relieving, and toxins counteracting effects as folk medicine in CM. This paper systematically reviewed the research advancement of the pharmacological effects of Cynanchum paniculatum among a variety of human diseases, including diseases of the respiratory, circulatory, digestive, urogenital, hematopoietic, endocrine and metabolomic, neurological, skeletal, and rheumatological systems and malignant diseases. This review aims to link the long history of clinical applications of Cynanchum paniculatum in CM with recent biomedical investigations. The major bioactive chemical compositions of Cynanchum paniculatum and their associated action mechanism unveiled by biomedical investigations as well as the present clinical applications and future perspectives are discussed. The major focuses of this review are on the diverse mechanisms of Cynanchum paniculatum and the role of its active components in inflammatory diseases.

show abstract

Paeonol attenuates acute lung injury by inhibiting HMGB1 in lipopolysaccharide-induced shock rats

Cited by 29 publications

References 37 publications

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

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

Mechanism of HMGB1–RAGE in Kawasaki disease with coronary artery injury

Cynanchum paniculatum and Its Major Active Constituents for Inflammatory‐Related Diseases: A Review of Traditional Use, Multiple Pathway Modulations, and Clinical Applications

Contact Info

Product

Resources

About