Paeoniflorin inhibits mast cell–mediated allergic inflammation in allergic rhinitis

Wang, Guanghui; Cheng, Nan

doi:10.1002/jcb.27135

Cited by 19 publications

(9 citation statements)

References 26 publications

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“…12 It can aggravate damage of nasal mucosa by degranulation and release large numbers of inflammatory transmitters. Many inflammation factors are involved in the progression of AR, although the mechanisms remain unclear 13 , 14 Our results indicated that polymorphisms of the VDR gene Fok I locus are associated with AR, and the A allele of FokI/rs22285570 increases the risk for AR; The Fok I/rs22285570 polymorphism also affects serum levels VDR mRNA. The IL-6, IL-8, and IL-10 levels were elevated in the AR group, indicating that inflammation plays an important in the pathophysiology of AR.…”

Section: Discussionmentioning

confidence: 71%

<p>Association Between Vitamin D Receptor Gene Polymorphism rs2228570 and Allergic Rhinitis</p>

Zhang¹,

Xu²

2020

PGPM

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Background: Vitamin D receptor (VDR) gene polymorphisms are involved in a variety of immune-related diseases, and VDR is associated with allergic rhinitis. The present study explored the associations between VDR gene polymorphisms and allergic rhinitis in the Chinese population. Methods: The study population consisted of 400 patients with allergic rhinitis and 400 healthy controls. General characteristics were determined by interview. Blood DNA was extracted and genotyping was performed via matrix-assisted laser desorption/ionization timeof-flight mass spectrometry. The associations of each genetic variant with risk for AR were assessed by calculating the odds ratio (OR) with 95% confidence interval (95% CI). Results: No significant differences were observed in general characteristics between cases and controls. The distributions of genotypes at the rs2228570 locus of the VDR gene conformed to Hardy-Weinberg equilibrium. There was a significant difference in the distribution of rs2228570 genotype (P<0.001) between cases and controls. Compared to GG and GA genotypes, the AA genotype increased the risk of AR (OR=3.27, 95% CI: 2.10-5.11, P=0.000; OR=2.58, 95% CI:1.63-4.08, P<0.001). Similar results were also observed in the dominant model (OR=1.64, 95% CI:1.24-2.17, P<0.001) and codominant model (OR=2.95, 95% CI:1.93-4.51, P<0.001). The A allele was still associated with elevated risk gene for AR after adjusting for potential confounding factors. Subgroup analyses indicated an interaction between alcohol and rs2228570 in the risk of allergic rhinitis. The A allele also increased the risk for AR in the population without asthma (OR=1.85, 95% CI:1.46-2.34, P<0.001). Conclusion: VDR gene polymorphism is associated with AR, and the AA genotype of rs2228570 is associated with the increased risk of AR in the Chinese population.

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Section: Discussionmentioning

confidence: 71%

<p>Association Between Vitamin D Receptor Gene Polymorphism rs2228570 and Allergic Rhinitis</p>

Zhang¹,

Xu²

2020

PGPM

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“…As a monoterpene glycoside, paeoniflorin is the main active ingredient in the roots of Chinese traditional Chinese medicine paeoniflorin [10]. Numerous pharmacological experiments have proved that paeoniflorin has significant anti-inflammatory, immunomodulatory, analgesic, anticoagulant, and antioxidant effects [11,12]. However, the mechanism of paeoniflorin in MIRI is still unknown.…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin on Rat Myocardial Ischemia Reperfusion Injury of Protection and Mechanism Research

et al. 2019

Pharmacology

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Objective: To study the myocardial benefit effect and mechanism of paeoniflorin on myocardial ischemia reperfusion injury (MIRI) in rats. Methods: Hundred SD rats were randomly divided into 5 groups: sham group, model group, Paeoniflorin (15 mg/kg) group, Paeoniflorin (30 mg/kg) group, and Paeoniflorin (60 mg/kg) group. Myocardial ischemia reperfusion model was established in each group except the sham group. The myocardial infarction and morphological changes were measured by the TTC staining and HE staining respectively. Myocardial caspase-3 was detected by immunohistochemistry. In addition, the protein levels of Bcl-2 and Bax and the expression ratio of p-erk, p-jnk, and p-p38 were detected by Western blot. Myocardial superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were measured by the assay kit. Results: Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can obviously alleviate myocardial infarction caused by MIRI (p < 0.05). HE staining showed that the myocardial morphology in the treatment group was obviously better than that in the model group. WB and immunohistochemistry showed that Paeoniflorin (30 mg/kg) andPaeoniflorin (60 mg/kg) can significantly increase the reduced protein level of bcl-2 (p < 0.05) and reduce the increased protein level of caspase3, bax p-erk, p-jnk, and p-p38 caused by MIRI (p < 0.05). The activity of SOD was increased and the level of MDA was decreased after Paeoniflorin treatment. Conclusion: Paeoniflorin preconditioning has a protective effect on MIRI in rats. Its mechanism is related to reducing oxidative stress and apoptosis by inhibiting the expression of apoptosis-related signaling pathway.

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“…84 Another agent with the potential for inhibiting both FcεRI and MRFPRX2 signaling in mast cells is paeoniflorin, a bioactive component in peony flower extracts; the mast cell stabilizing action of this agent has been demonstrated both in mast cell cultures and in rodent allergy models. [85][86][87][88] The direct molecular target of its action in this regard has yet to be defined.…”

Section: Discussion On Nutraceutical Strategies For Mast Cell Stabilizationmentioning

confidence: 99%

Nutraceutical Aid for Allergies – Strategies for Down-Regulating Mast Cell Degranulation

McCarty¹,

Lerner²,

DiNicolantonio

et al. 2021

JAA

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Interactions of antigens with the mast cell FcεRI-IgE receptor complex induce degranulation and boost synthesis of pro-inflammatory lipid mediators and cytokines. Activation of spleen tyrosine kinase (Syk) functions as a central hub in this signaling. The tyrosine phosphatase SHP-1 opposes Syk activity; stimulation of NADPH oxidase by FcεRI activation results in the production of oxidants that reversibly inhibit SHP-1, up-regulating the signal from Syk. Activated AMPK can suppress Syk activation by the FcεRI receptor, possibly reflecting its ability to phosphorylate the FcεRI beta subunit. Cyclic GMP, via protein kinase G II, enhances the activity of SHP-1 by phosphorylating its C-terminal region; this may explain its inhibitory impact on mast cell activation. Hydrogen sulfide (H 2 S) likewise opposes mast cell activation; H 2 S can boost AMPK activity, up-regulate cGMP production, and trigger Nrf2-mediated induction of Phase 2 enzymes -including heme oxygenase-1, whose generation of bilirubin suppresses NADPH oxidase activity. Phycocyanobilin (PCB), a chemical relative of bilirubin, shares its inhibitory impact on NADPH oxidase, rationalizing reported anti-allergic effects of PCB-rich spirulina ingestion. Phase 2 inducer nutraceuticals can likewise oppose the up-regulatory impact of NADPH oxidase on FcεRI signaling. AMPK can be activated with the nutraceutical berberine. Highdose biotin can boost cGMP levels in mast cells via direct stimulation of soluble guanylate cyclase. Endogenous generation of H 2 S in mast cells can be promoted by administering N-acetylcysteine and likely by taurine, which increases the expression of H 2 S-producing enzymes in the vascular system. Mast cell stabilization by benifuuki green tea catechins may reflect the decreased surface expression of FcεRI.

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Paeoniflorin inhibits mast cell–mediated allergic inflammation in allergic rhinitis

Cited by 19 publications

References 26 publications

<p>Association Between Vitamin D Receptor Gene Polymorphism rs2228570 and Allergic Rhinitis</p>

<p>Association Between Vitamin D Receptor Gene Polymorphism rs2228570 and Allergic Rhinitis</p>

Paeoniflorin on Rat Myocardial Ischemia Reperfusion Injury of Protection and Mechanism Research

Nutraceutical Aid for Allergies – Strategies for Down-Regulating Mast Cell Degranulation

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