Quantification of polygalasaponin F in rat plasma using liquid chromatography–tandem mass spectrometry and its pharmacokinetics application

Zhou, Wenli; Zhang, Jiantao; Xu, Wei; Sun, Jinghui

doi:10.1002/bmc.3435

Cited by 4 publications

(2 citation statements)

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“…Polygala (P.) japonica herba, a traditional Chinese herb, has been used as an expectorant, antitussive, antibacterial, and ataractic agent (Zhang et al 1996). It is widely used in China to treat acute bronchitis, pharyngitis, pneumonia, amygdalitis, and respiratory tract infections in children (Zhou et al 2015). The compounds isolated from P. japonica so far mainly include saponins, flavonoids, xanthones, polysaccharides, etc.…”

Section: Introductionmentioning

confidence: 99%

“…Polygalasaponin F (PSF, C 53 H 86 O 23 , Fig. 1) is a triterpenoid saponin and is also one of the major active constituents of P. japonica used for the quality control of the medicine (Zhou et al 2015). Previous research has reported that PSF has anti-inflammatory effects and its mechanism is associated with the NF-κB signaling pathway (Wei et al 2014;Yan et al 2015;Wang et al 2008).…”

Section: Introductionmentioning

confidence: 99%

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Polygalasaponin F treats mice with pneumonia induced by influenza virus

Wang

Liu

et al. 2019

Inflammopharmacol

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Background Influenza is an acute viral respiratory illness that causes high morbidity and mortality globally. Therapeutic actions are limited to vaccines and a few anti-viral drugs. Polygala (P.) japonica herba is rich in Polygalasaponin F (PSF, C 53 H 86 O 23), used for acute bronchitis, pharyngitis, pneumonia, amygdalitis, and respiratory tract infections treatment in China. Hypercytokinemia is often correlated with severe pneumonia caused by several influenza viruses. PSF was reported to have anti-inflammatory effects and its mechanism is associated with the nuclear factor (NF)-κB signaling pathway. The action of PSF to alleviate pulmonary inflammation caused by influenza A virus (IAV) infection requires careful assessment. In the present study, we evaluated the effect and mechanism of PSF on mice with pneumonia caused by influenza H1N1 (A/ FM/1/47). Methods Mice were infected intranasally with fifteen 50% mouse lethal challenge doses (MLD 50) of influenza virus. BALB/c mice were treated with PSF or oseltamivir (oral administration) for 2 h post-infection and received concomitant treatment for 5 days after infection. On day 6 post-infection, 10 mice per group were killed to collect related samples, measure body weight and lung wet weight, and detect the viral load, cytokine, prostaglandins, pathological changes, and cell pathway protein expression in the lungs. In addition, the survival experiments were carried out to investigate the survival of mice. The expression profile of cell pathway proteins was detected and analyzed using a broad pathway antibody array and confirmed the findings from the array by western blotting. Results Polygalasaponin F and oseltamivir can protect against influenza viral infection in mice. PSF and oseltamivir significantly relieved the signs and symptoms, reduced body weight loss, and improved the survival rate of H1N1-infected mice. Moreover, PSF efficiently decreased the level of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-4, interferon (IFN)-γ, thromboxane A 2 (TXA 2), and prostaglandin E 2 (PGE 2) in lung tissues of mice infected with influenza virus (p < 0.05-0.01). Oseltamivir had a similar effect to lung cytokine of PSF, but did not decrease the levels of TXA 2 and PGE 2. There was a twofold or greater increase in four cell pathway protein, namely NF-κB p65 (2.68-fold), I-kappa-B-alpha (IκBα) (2.56-fold), and MAPK/ERK kinase 1 (MEK1) (7.15-fold) assessed in the array induced by influenza virus. Western blotting showed that the expression of these proteins was significantly decreased in lung after influenza virus challenge in PSF and oseltamivirtreated mice (p < 0.05-0.01). Conclusion Polygalasaponin F appears to be able to augment protection against IAV infection in mice via attenuation of pulmonary inflammatory responses. Its effect on IAV-induced pulmonary inflammation was associated with suppression of Raf/MEK/ERK and NF-κB expressions.

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Section: Introductionmentioning

confidence: 99%