Alpinumisoflavone attenuates lipopolysaccharide-induced acute lung injury by regulating the effects of anti-oxidation and anti-inflammation both <i>in vitro</i> and <i>in vivo</i>

Li, Peiying; Liang, Yu-Chia; Sheu, Ming‐Jyh; Huang, Shyh-Shyun; Chao, Che‐Yi; Kuo, Yueh‐Hsiung; Huang, Guan‐Jhong

doi:10.1039/c8ra04098b

Cited by 26 publications

(22 citation statements)

References 43 publications

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“…The dose of hispolon was selected according to a previous study. After 6 h, the animals were sacrificed and samples were collected [ 31 ].…”

Section: Methodsmentioning

confidence: 99%

“…The dose of hispolon was selected according to a previous study. After 6 h, the animals were sacrificed and samples were collected [31]. neutrophils and edema in the interstitial space of the alveolar wall were observed in the LPS group, indicative of alveolar epithelial cell damage.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…The determination of BALF nitrite level was measured using Griess reagent [31]. Briefly, we added equal volumes of Griess reagent and BALF solution and mixed.…”

Section: Nitrite Assaymentioning

confidence: 99%

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Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy

et al. 2020

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The anti-inflammatory effect of hispolon has identified it as one of the most important compounds from Sanghuangporus sanghuang. The research objectives were to study this compound using an animal model by lipopolysaccharide (LPS)-induced acute lung injury. Hispolon treatment reduced the production of the pro-inflammatory mediator NO, TNF-α, IL-1β, and IL-6 induced by LPS challenge in the lung tissues, as well as decreasing their histological alterations and protein content. Total cell number was also reduced in the bronchoalveolar lavage fluid (BALF). Moreover, hispolon inhibited iNOS, COX-2 and IκB-α and phosphorylated IKK and MAPK, while increasing catalase, SOD, GPx, TLR4, AKT, HO-1, Nrf-2, Keap1 and PPARγ expression, after LPS challenge. It also regulated apoptosis, ER stress and the autophagy signal transduction pathway. The results of this study show that hispolon regulates LPS-induced ER stress (increasing CHOP, PERK, IRE1, ATF6 and GRP78 protein expression), apoptosis (decreasing caspase-3 and Bax and increasing Bcl-2 expression) and autophagy (reducing LC3 I/II and Beclin-1 expression). This in vivo experimental study suggests that hispolon suppresses the LPS-induced activation of inflammatory pathways, oxidative injury, ER stress, apoptosis and autophagy and has the potential to be used therapeutically in major anterior segment lung diseases.

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“…The dose of hispolon was selected according to a previous study. After 6 h, the animals were sacrificed and samples were collected [ 31 ].…”

Section: Methodsmentioning

confidence: 99%

Section: Experimental Protocolsmentioning

confidence: 99%

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Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy

et al. 2020

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“…Alpinumisoflavone (AIF) is a pyranoisoflavone isoflavone, and one of the major bioactive ingredient derived from the unripe fruits of C. tricuspidata [3,4,5,6]. AIF exhibits numerous beneficial pharmacological activities such as osteoprotective [7], antibacterial [8], estrogenic [9], anti-metastatic [10], atheroprotective [11], and antioxidant [12] effects. Moreover, considerable evidence has shown that AIF possesses in vitro and in vivo anticancer activities [3,13].…”

Section: Introductionmentioning

confidence: 99%

“…Namkoong et al revealed that AIF suppressed the nuclear factor (NF)-κB pathway and extracellular signal-regulated kinases (ERKs)/mitogen-activated protein kinase (MAPK) and induced apoptosis of lung cancer cells [3]. AIF is also known to attenuate lipopolysaccharide-induced acute lung injury by regulating the effects of antioxidation and anti-inflammation both in vitro and in vivo [12]. Gao et al [4] found that AIF impaired the metastatic potential of human melanoma (A375 and SK-MEL-1) cells by upregulating cell differentiation, as assessed based on melanin content, protoporphyrin IX accumulation, and tissue transglutaminase activity [4].…”

Section: Introductionmentioning

confidence: 99%

Physicochemical, Pharmacokinetic, and Toxicity Evaluation of Methoxy Poly(ethylene glycol)-b-Poly(d,l-Lactide) Polymeric Micelles Encapsulating Alpinumisoflavone Extracted from Unripe Cudrania tricuspidata Fruit

Lee

et al. 2019

Pharmaceutics

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Alpinumisoflavone, a major compound in unripe Cudrania tricuspidata fruit is reported to exhibit numerous beneficial pharmacological activities, such as osteoprotective, antibacterial, estrogenic, anti-metastatic, atheroprotective, antioxidant, and anticancer effects. Despite its medicinal value, alpinumisoflavone is poorly soluble in water, which makes it difficult to formulate and administer intravenously (i.v.). To overcome these limitations, we used methoxy poly(ethylene glycol)-b-poly(d,l-lactide) (mPEG-b-PLA) polymeric micelles to solubilize alpinumisoflavone and increase its bioavailability, and evaluated their toxicity in vivo. Alpinumisoflavone-loaded polymeric micelles were prepared using thin-film hydration method, and their physicochemical properties were characterized for drug release, particle size, drug-loading (DL, %), and encapsulation efficiency (EE, %). The in vitro drug release profile was determined and the release rate of alpinumisoflavone from mPEG-b-PLA micelles was slower than that from drug solution, and sustained. Pharmacokinetic studies showed decreased total clearance and volume of distribution of alpinumisoflavone, whereas area under the curve (AUC) and bioavailability were significantly increased by incorporation in mPEG-b-PLA micelles. In vivo toxicity assay revealed that alpinumisoflavone-loaded mPEG-b-PLA micelles had no severe toxicity. In conclusion, we prepared an intravenous (i.v.) injectable alpinumisoflavone formulation, which was solubilized using mPEG-b-PLA micelles, and determined their physicochemical properties, pharmacokinetics, and toxicity profiles.

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Astringin protects LPS-induced toxicity by suppressing oxidative stress and inflammation via suppression of PI3K/AKT/NF-κB pathway for pediatric acute lung injury

Wang

Jiang

et al. 2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Alpinumisoflavone attenuates lipopolysaccharide-induced acute lung injury by regulating the effects of anti-oxidation and anti-inflammation both in vitro and in vivo

Abstract: The present study demonstrated that alpinumisoflavone exerts the significant effects of anti-inflammatory and anti-oxidative in both LPS-induced RAW264.7 macrophages and a mouse model of acute lung injury.

Cited by 26 publications

References 43 publications

Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy

Attenuation of Lipopolysaccharide-Induced Acute Lung Injury by Hispolon in Mice, Through Regulating the TLR4/PI3K/Akt/mTOR and Keap1/Nrf2/HO-1 Pathways, and Suppressing Oxidative Stress-Mediated ER Stress-Induced Apoptosis and Autophagy

Physicochemical, Pharmacokinetic, and Toxicity Evaluation of Methoxy Poly(ethylene glycol)-b-Poly(d,l-Lactide) Polymeric Micelles Encapsulating Alpinumisoflavone Extracted from Unripe Cudrania tricuspidata Fruit

Astringin protects LPS-induced toxicity by suppressing oxidative stress and inflammation via suppression of PI3K/AKT/NF-κB pathway for pediatric acute lung injury

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