Dietary Monascus adlay supplements facilitate suppression of cigarette smoke-induced pulmonary endoplasmic reticulum stress, autophagy, apoptosis and emphysema-related PLGF in the rat

Li, Ping Chia; Tsai, Wen Hsin; Chien, Chiang Ting

doi:10.1016/j.foodchem.2012.08.007

Cited by 10 publications

(30 citation statements)

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“…Monascus fermented products were prepared on an adlay substrate, using a solid-state culture method as described previously [4,11]. In brief, adlay (obtained from the Erhlin Farmers' Association, Changhua County, Taiwan) was immersed in deionized water for 2 h, dried and autoclaved at 121°C for 20 min.…”

Section: Preparation Of Monascus Adlay (Ma)mentioning

confidence: 99%

“…The dried MA was ground into a coarse powder (20 mesh) using a Restsch Ultra Centrifugal Mill and Sieving Machine (Haan, Germany). Our previous report had indicated the MK content in MA extract by a high-performance liquid chromatography (HPLC) [11]. Briefly, 1 g of powdered MA was extracted with 5 mL ethyl acetate at 70°C for 1.5 h. After 5 min of centrifugation at 1800 rpm and filtration through a 0.45-µm membrane, the filtrate was dried under a vacuum.…”

Section: Preparation Of Monascus Adlay (Ma)mentioning

confidence: 99%

“…The standard rat chow diet contained 58% carbohydrates, 28.5% proteins, and 13.5% fat (Laboratory Rodent diet 5001; Young Li Trading Company Ltd., Sijhih City, New Taipei City, Taiwan). We mixed powdered rat chow diet and powdered MA at a ratio of 99:1 by combining them through a 20-mesh sieve (aperture = 0.94 mm) [11]. We used 2% corn starch and 3% soybean oil to re-form the product into the MA lump diet.…”

Section: Animals and Ma Treatmentsmentioning

confidence: 99%

“…produces monascus adlay (MA) containing both functional and active components [11]. MA extracts including rich MK and total phenol contents display higher antioxidant activity, reducing power, scavenging and chelating abilities than uninoculated adlay products [5,11].…”

mentioning

confidence: 99%

“…MA extracts including rich MK and total phenol contents display higher antioxidant activity, reducing power, scavenging and chelating abilities than uninoculated adlay products [5,11]. MA and MK can depress oxidative stress evoked endoplasmic reticulum stress, apoptosis, autophagy and pyroptosis [11]. MK or lovastatin can inhibit urotensin enhanced expression of VCAM-1 and ICAM-1 by modulating the Rho activation, and NF-kB inhibitors [12].…”

mentioning

confidence: 99%

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Monascus Adlay and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

Tien¹,

Chueh²,

Hsia³

et al. 2016

Kidney Blood Press Res

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Background/Aims: Monascus Adlay (MA) prepared from fungal fermentation of Monascus purpureus inoculating with cooked adlay contains high content of monakolin K (MK) and phenolic compounds. We explored whether MA and MK improve FeCl₃-induced arterial thrombosis in rats. Methods: The rats were divided into control, FeCl₃-treated rat carotid artery occlusion (TTO), TTO determined with one-week MA, and TTO determined with one-week MK. We compared MA or MK effects on oxidative stress by chemiluminescence amplification and immunohistochemistry, TTO by a transonic system, NFκB, ICAM-1, endoplasmic reticulum stress CHOP and Nrf2 signaling by western blotting. Results: MA or MK efficiently depressed O₂^-, H₂O₂ and HOCl levels, platelet activation and aggregation and H₂O₂-enhanced ICAM-1 and VCAM-1 expression in the endothelial cells. FeCl₃ significantly increased NFκB p65, 3-nitrotyrosine, CHOP and ICAM-1 expression, and decreased nuclear Nrf2 translocation and induces arterial thrombus formation. MA or MK pretreatment significantly elongated the level of FeCl₃-induced TTO compared to TTO group, significantly decreased proinflammatory NF-κB/ICAM-1 signaling, endoplasmic reticulum stress CHOP expression and decreased thrombotic area. MA or MK significantly preserved nuclear Nrf2 translocation. MA and MK exerted a similar protective effect in attenuating thrombus formation. Conclusions: We suggest MA is better than MK to improve FeCl₃-induced arterial thrombosis.

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Section: Preparation Of Monascus Adlay (Ma)mentioning

confidence: 99%

Section: Preparation Of Monascus Adlay (Ma)mentioning

confidence: 99%

Section: Animals and Ma Treatmentsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Monascus Adlay and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

Tien¹,

Chueh²,

Hsia³

et al. 2016

Kidney Blood Press Res

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Natural products in the treatment of pulmonary emphysema: Therapeutic effects and mechanisms of action

et al. 2022

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Elastase induced lung epithelial cell apoptosis and emphysema through placenta growth factor

et al. 2013

Cell Death Dis

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Chronic pulmonary obstructive disease (COPD) is the fourth leading cause of death worldwide, however, the pathogenic factors and mechanisms are not fully understood. Pulmonary emphysema is one of the major components of COPD and is thought to result from oxidative stress, chronic inflammation, protease–antiprotease imbalance and lung epithelial (LE) cell apoptosis. In our previous studies, COPD patients were noted to have higher levels of placenta growth factor (PlGF) in serum and bronchoalveolar lavage fluid than controls. In addition, transgenic mice overexpressing PlGF developed pulmonary emphysema and exposure to PlGF in LE cells induced apoptosis. Furthermore, intratracheal instillation of porcine pancreatic elastase (PPE) on to PlGF wild type mice induced emphysema, but not in PlGF knockout mice. Therefore, we hypothesized that PPE generates pulmonary emphysema through the upregulation of PlGF expression in LE cells. The elevation of PlGF then leads to LE cell apoptosis. In the present study, we investigated whether PPE induces PlGF expression, whether PlGF induces apoptosis and whether the downstream mechanisms of PlGF are related to LE cell apoptosis. We found that PPE increased PlGF secretion and expression both in vivo and in vitro. Moreover, PlGF-induced LE cell apoptosis and PPE-induced emphysema in the mice were mediated by c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) pathways. Given these findings, we suggest that the increase in PlGF and PlGF-induced JNK and p38 MAPK pathways contribute to PPE-induced LE cell apoptosis and emphysema. Regulatory control of PlGF and agents against its downstream signals may be potential therapeutic targets for COPD.

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Dietary Monascus adlay supplements facilitate suppression of cigarette smoke-induced pulmonary endoplasmic reticulum stress, autophagy, apoptosis and emphysema-related PLGF in the rat

Cited by 10 publications

References 30 publications

<b><i>Monascus Adlay</i></b> and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

<b><i>Monascus Adlay</i></b> and Monacolin K Attenuates Arterial Thrombosis in Rats through the Inhibition of ICAM-1 and Oxidative Stress

Natural products in the treatment of pulmonary emphysema: Therapeutic effects and mechanisms of action

Elastase induced lung epithelial cell apoptosis and emphysema through placenta growth factor

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