The pharmacological properties and corresponding mechanisms of farrerol: a comprehensive review

Qin, Xiaojiang; Xu, Xin; Hou, Xiaomin; Liang, Ru‐Ping; Chen, Liangjing; Hao, Yuxuan; Gao, Anqi; Du, Xuewen; Zhao, Liangyuan; Shi, Yiwei; Liu, Qingshan

doi:10.1080/13880209.2021.2006723

Cited by 9 publications

(3 citation statements)

References 91 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The relationship between Farrerol and oxidative stress has been studied. Farrerol can affect the occurrence and development of diseases by regulating NOX4/ROS/ERK/TGF-β signaling pathway, NRF2/Keap1 signaling pathway, HO-1 and NQO1 signaling pathway ( Qin et al, 2022 ; Chen et al, 2020 ; Ma et al, 2019 ). In this paper, we found that Farrerol could inhibit the expression of DHE, mitoSOX and the expression of NOX2.…”

Section: Discussionmentioning

confidence: 99%

Farrerol prevents Angiotensin II-induced cardiac remodeling in vivo and in vitro

Wang

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Cardiovascular disease has become the primary disease that threatens human health and is considered the leading cause of death. Cardiac remodeling, which is associated with cardiovascular disease, mainly manifests as cardiac hypertrophy, fibrosis, inflammation, and oxidative stress. Farrerol plays an important role in treating conditions such as inflammation, endothelial injury and tumors, and we speculated that Farrerol may also play an important role in mitigating cardiac hypertrophy and remodeling. We established a model of myocardial remodeling using Angiotensin II (Ang II) with concurrent intraperitoneal injection of Farrerol as an intervention. We used cardiac ultrasound, immunohistochemistry, Immunofluorescence, Wheat Germ Agglutinin, Dihydroethidium, Western Blot, qPCR and other methods to detect the role of Farrerol in cardiac remodeling. The results showed that Farrerol inhibited Ang II-induced cardiac hypertrophy; decreased the ratio of heart weight to tibia length in mice; reduced inflammation, fibrosis, and oxidative stress; and reduced the size of cardiomyocytes in vivo. Farrerol inhibited Ang II-induced cardiomyocyte hypertrophy, levels of oxidative stress, and the proliferation and migration of fibroblast in vitro. Our results revealed that Farrerol could inhibit Ang II-induced cardiac remodeling. Farrerol may therefore be a candidate drug for the treatment of myocardial remodeling.

show abstract

Section: Discussionmentioning

confidence: 99%

Farrerol prevents Angiotensin II-induced cardiac remodeling in vivo and in vitro

Wang

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

show abstract

“…FA, found to be naturally present in Rhododendron dauricum L . leaves, is a natural dihydro flavonoid active substance with antibacterial, anti-inflammatory, antioxidant, and other biological activities ( Li et al, 2013 ; Ran et al, 2018 ; Li et al, 2019 ; Qin et al, 2022 ). In this study, we aimed to find its role and mechanism in I/R-induced injury.…”

Section: Discussionmentioning

confidence: 99%

Farrerol Alleviates Myocardial Ischemia/Reperfusion Injury by Targeting Macrophages and NLRP3

2022

View full text Add to dashboard Cite

Myocardial ischemia/reperfusion (I/R) injury is associated with high mortality and morbidity, however, it has no curative treatment. Farrerol (FA), an active compound extracted from rhododendron, has antibacterial, anti-inflammatory, and antioxidant activities, but its effect and mechanism of FA in I/R injury remain unclear. Here, we found that FA alleviated myocardial I/R in vivo, and decreased the secretion of myocardial injury factors (CK-MB, LDH, troponin-1, and NT-proBNP) while inhibiting the release of inflammatory factors (IL-1β, IL-6, and TNF-α). FA could also alleviate excessive oxidative stress by elevating the level of antioxidant enzymes and reducing oxidation products; and decreased reduced the expression of apoptosis-associated proteins (cleaved caspase-3, Bax, and Bcl-2). However, inhibiting the autophagic pathway or knocking out the Nrf2 gene did not eliminate the myocardial protective effect of FA, but interestingly, macrophage clearance and Nlrp3 deficiency effectively blocked the myocardial protective effect of FA. In addition, FA suppressed NLRP3 inflammasome activation by interfering with NLRP3 and NEK7. In conclusion, these results support drug-targeted macrophage therapy for myocardial I/R and indicate that FA may be used as an immunomodulator in clinical therapy for myocardial I/R.

show abstract

“…Then TRPV1 played a regulatory role on TRPA1. Numerous molecules within the network targeted by JZOL for cough treatment have been previously linked to cough, for example, JNK was a common molecule in many respiratory diseases, like asthma and acute lung injury, and participated in many pathogenic molecular pathways [54][55][56] . PKA and PKC activation of TRPV1 induced cough and served as an inflammatory marker in evaluating the airway in a postoperative chronic cough model 57,58 .…”

Section: The Role Of Jzol In the Treatment Of Coughmentioning

confidence: 99%

Depicting the regulatory role of JZOL on TRP channels in the treatment of Acute Bronchitis based on the combination of clinical trials, computational analysis and in vivo experiments

Fan,

Wu,

et al. 2024

Preprint

View full text Add to dashboard Cite

The comparison between traditional Chinese medicine Jinzhen Oral Liquid (JZOL) and western medicine in treating children with acute bronchitis (AB) showed encouraging outcomes. This trial evaluated the efficacy and safety of the JZOL for improving cough and expectoration in children with AB. 480 children were randomly assigned to take JZOL or Ambroxol Hydrochloride and Clenbuterol Hydrochloride Oral Solution for 7 days. The primary outcome was time-to-cough resolution. The median time-to-cough resolution in both groups was 5.0 days and the antitussive onset median time was only 1 day. This head to head randomized controlled trial showed that JZOL was not inferior to cough suppressant and phlegm resolving western medicine in treating cough and sputum and could comprehensively treat respiratory and systemic discomfort symptoms. Combined with clinical trials, the mechanism of JZOL against AB was uncovered by network target analysis, it was found that the pathways in TRP channels like IL-1β;/IL1R/TRPV1/TRPA1, NGF/TrkA/TRPV1/TRPA1 and PGE2/EP/PKA/TRPV1/TRPA1 might play important roles. Animal experiments further confirmed that inflammation and immune regulatory effect of JZOL in the treatment of AB were of vital importance and TRP channels was the key mechanism of action.

show abstract

The pharmacological properties and corresponding mechanisms of farrerol: a comprehensive review

Cited by 9 publications

References 91 publications

Farrerol prevents Angiotensin II-induced cardiac remodeling in vivo and in vitro

Farrerol prevents Angiotensin II-induced cardiac remodeling in vivo and in vitro

Farrerol Alleviates Myocardial Ischemia/Reperfusion Injury by Targeting Macrophages and NLRP3

Depicting the regulatory role of JZOL on TRP channels in the treatment of Acute Bronchitis based on the combination of clinical trials, computational analysis and in vivo experiments

Contact Info

Product

Resources

About