Effect of Magnolol onin VitroMitochondrial Lipid Peroxidation and Isolated Cold-Preserved Warm-Reperfused Rat Livers

Chiu, Jen‐Hwey; Wang, Juo-Chi; Lui, Wing‐Yiu; Wu, Chew-Wun; Hong, Chuang‐Ye

doi:10.1006/jsre.1998.5455

Cited by 26 publications

(16 citation statements)

References 22 publications

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“…Furthermore, it is an effective scavenger of free radicals such as hydroxyl radicals (Taira et al, 1993), is able to inhibit UV-induced mutation (Fujita and Taira, 1994) and attenuates peroxidative damage and improves survival of rats with sepsis (Kong et al, 2000). In vitro, magnolol is proved to be an effective anti-oxidant and suppresses lipid peroxidation in rat liver mitochondria (Chiu et al, 1999). Our results showed that after treatment with different doses of magnolol, the increased ALT, AST, LDH, and TBARS levels induced by APAP were attenuated.…”

Section: Discussionmentioning

confidence: 97%

“…Magnolol, an antioxidant purified from M. officinalis, is approximately 1,000 times more potent than α-tocopherol (Hong et al, 1996, Lo et al, 1994 in inhibiting lipid peroxidation in heart mitochondria and 340 times more potent in rat liver mitochondria (Chiu et al, 1999). In addition, magnolol has been demonstrated to suppress polymorphonuclear leukocyte infiltration in a mouse model of ionophore A23187-induced pleurisy and to reduce leukotriene B formation in rat-isolated peripheral neutrophil suspension (Wang et al, 1992) and in rat basophilic leukemia-2H3 cells (Hamasaki et al, 1999).…”

Section: Introductionmentioning

confidence: 98%

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Antioxidative and hepatoprotective effects of magnolol on acetaminophen-induced liver damage in rats

et al. 2009

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Acute liver failure (ALF), an often fatal condition characterized by massive hepatocyte necrosis, is frequently caused by drug poisoning, particularly with acetaminophen (N-acetyl-p-aminophenol/APAP). Hepatocyte necrosis is consecutive to glutathione (GSH) depletion and mitochondrial damage caused by reactive oxygen species (ROS) overproduction. Magnolol, one major phenolic constituent of Magnolia officinalis, have been known to exhibit potent antioxidative activity. In this study, the anti-hepatotoxic activity of magnolol on APAP-induced toxicity in the Sprague-Dawley rat liver was examined. After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 mug/kg). Histological changes around the hepatic central vein, lipid peroxidation (thiobarbituric acid-reactive substance/TBARS), and GSH depletion in liver tissue induced by APAP were also recovered by magnolol treatment. The data show that oxidative stress followed by lipid peroxidation may play a very important role in the pathogenesis of APAP-induced hepatic injury; treatment with lipid-soluble antioxidant, magnolol, exerts anti-hepatotoxic activity. Our study points out the potential interest of magnolol in the treatment of toxic ALF.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

Antioxidative and hepatoprotective effects of magnolol on acetaminophen-induced liver damage in rats

et al. 2009

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“…Both oxidative stress and inflammation cause fibrosis, which can be prevented by attenuation of transforming growth factor beta 1 (TGF- β 1) and its downstream profibrotic factors such as connective tissue growth factor (CTGF) through inhibition of Smad-2/3 signaling pathway [21]. Furthermore, it was reported that magnolol regulated lipid metabolism by increase of fatty acid β -oxidation and lipolysis, finally reducing lipid accumulation in the tissue [22, 23]. …”

Section: Introductionmentioning

confidence: 99%

BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress

Wang

Zhang

et al. 2014

Oxidative Medicine and Cellular Longevity

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The present study was to investigate whether a magnolia extract, named BL153, can prevent obesity-induced liver damage and identify the possible protective mechanism. To this end, obese mice were induced by feeding with high fat diet (HFD, 60% kcal as fat) and the age-matched control mice were fed with control diet (10% kcal as fat) for 6 months. Simultaneously these mice were treated with or without BL153 daily at 3 dose levels (2.5, 5, and 10 mg/kg) by gavage. HFD feeding significantly increased the body weight and the liver weight. Administration of BL153 significantly reduced the liver weight but without effects on body weight. As a critical step of the development of NAFLD, hepatic fibrosis was induced in the mice fed with HFD, shown by upregulating the expression of connective tissue growth factor and transforming growth factor beta 1, which were significantly attenuated by BL153 in a dose-dependent manner. Mechanism study revealed that BL153 significantly suppressed HFD induced hepatic lipid accumulation and oxidative stress and slightly prevented liver inflammation. These results suggest that HFD induced fibrosis in the liver can be prevented partially by BL153, probably due to reduction of hepatic lipid accumulation, inflammation and oxidative stress.

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“…Saiboku-to, a herbal medicine for bronchial asthma, consists of a number of different herbs, one of which is Magnolia officinalis. 1 It has been reported that this compound inhibits the respiratory burst in formylmethionyl-leucyl-phenylalanine activated neutrophils, 2 suppresses the overproduction of nitric oxide and tumour necrosis factor (TNF)-α in lipopolysaccharide activated macrophages, 3 protects transplanted organs from lipid peroxidation, 4 and prevents cortical neurons from chemical hypoxia in rats. 5 Several studies have shown that magnolol exerts an antioxidative effect on neutrophil adhesion in vitro and in septic rats.…”

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confidence: 99%

Stimulation of the BKCa channel in cultured smooth muscle cells of human trachea by magnolol

Chen

et al. 2002

Thorax

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Background: Magnolol, a compound isolated from the cortex of Magnolia officinalis, has been found to possess anti-allergic and anti-asthmatic activity. Methods: The effect of magnolol on ionic currents was studied in cultured smooth muscle cells of human trachea with the aid of the patch clamp technique. Results: In whole cell current recordings magnolol reversibly increased the amplitude of K + outward currents. The increase in outward current caused by magnolol was sensitive to inhibition by iberiotoxin (200 nM) or paxilline (1 µM) but not by glibenclamide (10 µM). In inside out patches, magnolol added to the bath did not modify single channel conductance but effectively enhanced the activity of large conductance Ca 2+ activated K + (BK Ca ) channels. Magnolol increased the probability of these channel openings in a concentration dependent manner with an EC 50 value of 1.5 µM. The magnolol stimulated increase in the probability of channels opening was independent of internal Ca 2+ . The application of magnolol also shifted the activation curve of BK Ca channels to less positive membrane potentials. The change in the kinetic behaviour of BK Ca channels caused by magnolol in these cells is the result of an increase in dissociation and gating constants. Conclusions: These results provide evidence that, in addition to the presence of antioxidative activity, magnolol is potent in stimulating BK Ca channel activity in tracheal smooth muscle cells. The direct stimulation of these BK Ca channels by magnolol may contribute to the underlying mechanism by which it acts as an anti-asthmatic compound.

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Effect of Magnolol onin VitroMitochondrial Lipid Peroxidation and Isolated Cold-Preserved Warm-Reperfused Rat Livers

Cited by 26 publications

References 22 publications

Antioxidative and hepatoprotective effects of magnolol on acetaminophen-induced liver damage in rats

Antioxidative and hepatoprotective effects of magnolol on acetaminophen-induced liver damage in rats

BL153 Partially Prevents High-Fat Diet Induced Liver Damage Probably via Inhibition of Lipid Accumulation, Inflammation, and Oxidative Stress

Stimulation of the BKCa channel in cultured smooth muscle cells of human trachea by magnolol

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