Modulatory effect of anisodamine on airway hyper-reactivity and eosinophilic inflammation in a murine model of allergic asthma

Xu, Zu-Peng; Wang, Hao; Hou, Liang; Zheng, Xiaoli; Zhu, Liang; Chen, Hongzhuan; Cui, Yong-Yao

doi:10.1016/j.intimp.2010.12.001

Cited by 20 publications

(17 citation statements)

References 32 publications

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“…It was previously reported that Ani played an alleviative role in airway hyper-reactivity and inflammation in a mouse model of allergic asthma through the modulation of Th1/Th2 balance12. Several works from our laboratory have demonstrated the modulatory effects of Ani on inflammatory response in inflammatory and autoimmune diseases913.…”

Section: Discussionmentioning

confidence: 91%

“…Ani, extracted from a traditional Chinese herb Scopolia taugutica , acts as an antagonist for muscarinic cholinergic receptor, less toxic on CNS compared with atropine912. It was previously reported that Ani played an alleviative role in airway hyper-reactivity and inflammation in a mouse model of allergic asthma through the modulation of Th1/Th2 balance12.…”

Section: Discussionmentioning

confidence: 99%

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Combined administration of anisodamine and neostigmine rescued acute lethal crush syndrome through α7nAChR-dependent JAK2-STAT3 signaling

Shao

Peng

et al. 2016

Sci Rep

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Previously we showed that Ani (anisodamine)/Neo (neostigmine) combination produced anti-shock effect via activating α7 nicotinic acetylcholine receptor (α7nAChR). In this study, we aim to investigate the therapeutic effect and underlying mechanisms of Ani/Neo combination in acute lethal crush syndrome (CS). In rat and rabbit CS models, Ani/Neo combination increased the 24 h survival rates, improved hemodynamics and decreased the levels of creatine kinase, MB isoenzyme of creatine kinase, blood urea nitrogen, creatinine, K+ in serum. It also decreased the levels of H2O2, myeloperoxidase (MPO) and nitric oxide (NO) in serum and compressed muscle in rat CS model. In wild-type (WT) mice with CS, Ani/Neo combination increased 24 h survival rate and decreased the levels of H2O2, MPO, NO, TNFα, IL-6 and IL-10 in compressed muscle. These effects were attenuated by α7nAChR knockout (KO). Moreover, Ani/Neo combination prevented the decrease of phosphorylation of Janus kinase 2 (JAK2) and phosphorylation of signal transducer and activator of transcription 3 (STAT3) induced by CS. These effects of Ani/Neo in CS mice were cancelled by methyllycaconitine (α7nAChR antagonist) and α7nAChR KO. Collectively, our results demonstrate that Ani/Neo combination could produce therapeutic effects in CS. The underlying mechanism involves the activation of α7nAChR-dependent JAK2-STAT3 signaling pathway.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Combined administration of anisodamine and neostigmine rescued acute lethal crush syndrome through α7nAChR-dependent JAK2-STAT3 signaling

Shao

Peng

et al. 2016

Sci Rep

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“…In a mouse model of ovalbumin‐induced asthma, anisodamine was shown to significantly suppress the peribronchial and perivascular infiltration and accumulation of eosinophils in the airways, similar to the effects of atropine and dexamethasone (Xu et al ., ). This indicates the probable involvement of muscarinic receptors in airway inflammation following eosinophil infiltration.…”

Section: Pulmonary Effectsmentioning

confidence: 97%

“…Because anisodamine prevented bronchial contractile responses only following ovalbumin challenge, this may indicate that ACh affects inflamed airway smooth muscle. ACh is known to promote the release of cytokines from epithelial and smooth muscle cells during inflammation, which in turn attract inflammatory cells to the airways and induce remodelling of the tissue (Gosens et al ., ; Xu et al ., ; Kolahian and Gosens, ). In this study, anisodamine had a similar effect as atropine in that it attenuated eosinophilic airway inflammation and affected the balance of Th1/Th2 lymphocytes, suppressing the Th2‐mediated immune response and enhancing the Th1‐mediated immune response (down‐regulation of Th2‐associated IL‐4 and up‐regulation of Th1‐associated IFNγ, respectively) (Xu et al ., ).…”

Section: Pulmonary Effectsmentioning

confidence: 97%

“…Current in vitro and animal model studies have demonstrated that anisodamine has beneficial effects in a variety of disease conditions of different aetiologies and in various organs. These include cardiac arrhythmias (Chen and Gu, ; Yang et al ., ), acute lung injury (Zhang et al ., ), asthma (Xu et al ., ), arthritis (Zhou et al ., ) and septic shock (Zhao et al ., ). It was found to be protective at cellular, organ system and animal levels in inflammation (Liu et al ., ; Xu et al ., ; You et al ., ), oxidative stress (Luo et al ., ; Esberg and Ren, ; Liu et al ., ), coagulopathy (Xiu et al ., ; Ruan et al ., ) and molecular signalling pathways (Norby and Ren, ; Xing et al ., ).…”

Section: Introductionmentioning

confidence: 99%

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Possible role for anisodamine in organophosphate poisoning

Eisenkraft

Falk

2016

British J Pharmacology

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In cases of organophosphate poisoning, patients are treated with a combination of antidotes. In addition to these poison‐directed antidotes, patients may require extra oxygen and artificial ventilation; other modalities may also be needed due to the wide range of toxic effects. Anisodamine is a belladonna alkaloid, and like other drugs from this family is non subtype‐selective muscarinic, and a nicotinic cholinoceptor antagonist, which has been employed in traditional Chinese medicine. As a muscarinic antagonist, it displays similar pharmacological effects to atropine and scopolamine. However, anisodamine is not only less potent than atropine and scopolamine but also less toxic. Current in vitro and animal model studies have demonstrated that anisodamine has protective effects in a variety of diseases. Organophosphate poisoning involves not only the central and peripheral nervous systems, but also the cardiac and respiratory systems, as well as activation of inflammatory processes and oxidative stress. Therefore, the anticholinergic and additional activities of anisodamine appear to be relevant and justify its consideration as an addition to the existing remedies. However, more research is needed, as at present data on the role of anisodamine in the management of organophosphate poisoning are limited. Here, we review the beneficial effects of anisodamine on processes relevant to organophosphate poisoning.

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Anisodamine affects the pigmentation, mineral density, craniofacial area, and eye development in zebrafish embryos

Wang

Chen

Wang

et al. 2021

J of Applied Toxicology

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Anisodamine is one of the major components of the tropine alkaloid family and is widely used in the treatment of pain, motion sickness, pupil dilatation, and detoxification of organophosphorus poisoning. As a muscarinic receptor antagonist, the low toxicity and moderate drug effect of anisodamine often result in high doses for clinical use, making it important to fully investigate its toxicity. In this study, zebrafish embryos were exposed to 1.3-, 2.6-, and 5.2-mM anisodamine for 7 days to study the toxic effects of drug exposure on pigmentation, mineral density, craniofacial area, and eye development. The results showed that exposure to anisodamine at 1.3 mM resulted in cranial malformations and abnormal pigmentation in zebrafish embryos; 2.6-and 5.2-mM anisodamine resulted in significant eye development defects and reduced bone density in zebrafish embryos. The associated toxicities were correlated with functional development of neural crest cells through gene expression (col1a2, ddb1, dicer1, mab21l1, mab21l2, sox10, tyrp1b, and mitfa) in the dose of 5.2-mM exposed group. In conclusion, this study provides new evidence of the developmental toxicity of high doses of anisodamine in aqueous solutions to organisms and provides a warning for the safe use of this drug.

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Modulatory effect of anisodamine on airway hyper-reactivity and eosinophilic inflammation in a murine model of allergic asthma

Cited by 20 publications

References 32 publications

Combined administration of anisodamine and neostigmine rescued acute lethal crush syndrome through α7nAChR-dependent JAK2-STAT3 signaling

Combined administration of anisodamine and neostigmine rescued acute lethal crush syndrome through α7nAChR-dependent JAK2-STAT3 signaling

Possible role for anisodamine in organophosphate poisoning

Anisodamine affects the pigmentation, mineral density, craniofacial area, and eye development in zebrafish embryos

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