herbs of Phellinus igniarius
3-Hydroxy-2-methyl-4H-pyran-4-one/MALTENE/3-hydroxy-2-methyl-4-pyrone/3-Hydroxy-2-methyl-g-pyrone/Vetol/Palatone/Laricin/4H-Pyran-4-one, 3-hydroxy-2-methyl-/Talmon/3-Hydroxy-2-methyl-4-pyrone,Maltol/2-methyl-3-hydroxy-4H-pyran-4-one/MALTOL FCC/Veltol/Maltol/2-methyl-3-oxy-4H-pyran-4-one/2-methyl-3-hydroxy-4-pyranone
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provides coniferyl ferulate(CAS#:118-71-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Our previous study has confirmed that maltol can attenuate alcohol-induced acute hepatic damage and prevent oxidative stress in mice. Therefore, maltol might have the capacity to improve thioacetamide (TAA)-induced liver fibrosis. The purpose of this work was to explore the antifibrotic efficacy and underlying mechanisms of maltol for TAA-treated mice. Progressive liver fibrosis was established with a dose-escalating protocol in which the mice received TAA intraperitoneal three times a week for a total duration of 9 weeks. The injection doses of TAA were 50 mg/kg for the first week, 100 mg/kg for the second and third weeks, and 150 mg/kg for the rest of the injections. Maltol with doses of 50 and 100 mg/kg was given by gavage after 4 weeks of intraperitoneal injection of TAA, respectively, once daily for 5 weeks. Results indicated that TAA intraperitoneal injection significantly increased serum activities of alanine aminotransferase (ALT) (52.93 ± 13.21 U/L vs 10.22 ± 3.36 U/L) and aspartate aminotransferase (AST) (67.58 ± 25.84 U/L vs 39.34 ± 3.89 U/L); these elevations were significantly diminished by pretreatment with maltol. Additionally, maltol ameliorated TAA-induced oxidative stress with attenuation in MDA ( p < 0.05 or p < 0.01) content; evident elevation in the GSH levels, GSH/GSSG ratio ( p < 0.05 or p < 0.01), and superoxide dismutase (SOD) ( p < 0.01); and restored liver histology accompanied by a decrease of α-smooth muscle actin (α-SMA) expression. Furthermore, maltol significantly suppressed the transforming growth factor-β1 (TGF-β1) expression and the PI3K/Akt pathway. This study suggested that maltol alleviated experimental liver fibrosis by suppressing the activation of HSCs and inducing apoptosis of activated HSCs through TGF-β1-mediated PI3K/Akt signaling pathway. These findings further clearly suggested that maltol is a potent therapeutic candidate for the alleviation of liver fibrosis.
PI3K/Akt signaling pathway; apoptosis; hepatic fibrosis; maltol; thioacetamide.
Maltol Mitigates Thioacetamide-induced Liver Fibrosis Through TGF-β1-mediated Activation of PI3K/Akt Signaling Pathway
Xiao-Jie Mi 1 , Jin-Gang Hou 1 2 , Shuang Jiang 1 , Zhi Liu 1 , Shan Tang 1 , Xiang-Xiang Liu 1 , Ying-Ping Wang 1 3 , Chen Chen 4 , Zi Wang 1 , Wei Li 1 3
2019 Feb 6
Scope: Maltol (3-hydroxy-2-methy-4-pyrone), a potent antioxidative agent, typically is used to enhance flavor and preserve food. This study evaluated its effects on preventing diabetic peripheral neuropathy (DPN) in streptozotocin (STZ)-induced diabetic rats and explored its mechanisms.
Methods and results: We intraperitoneally injected Sprague-Dawley (SD) rats with STZ (65 mg kg-1, ip) and treated the rats with different doses of maltol after 4 weeks of injection. During treatment, we evaluated motor nerve conduction velocity (MNCV) and thermal and mechanical hyperalgesia and assayed the oxidative stress, Na+-K+-ATPase activity, and apoptosis. Repeated treatment with maltol for 12 weeks significantly improved thermal and mechanical hyperalgesia, increased the MNCV, elevated the Na+-K+-ATPase activity, and ameliorated oxidative stress and apoptosis in STZ-induced diabetic rats. We coincubated RSC96 cells, a Schwann cell line, with maltol and hydrogen peroxide (H2O2, 0.6 mM). Evidently, maltol increased cell viability and inhibited apoptosis after injury by H2O2.
Maltol was demonstrated to prevent DPN development and may provide a new alternative for the treatment of DPN.
Maltol, a Food Flavor Enhancer, Attenuates Diabetic Peripheral Neuropathy in Streptozotocin-Induced Diabetic Rats
Nan Guo 1 , Caina Li, Quan Liu, Shuainan Liu, Yi Huan, Xing Wang, Guoliang Bai, Miaomiao Yang, Sujuan Sun, Caimin Xu, Zhufang Shen
2018 Dec 13
Cisplatin, a potent anticancer drug, is usually causing nephrotoxicity; limiting its therapeutic application and efficiency. Maltol may be used to prevent such toxic effect. The aim of this study was to investigate the underlying protective mechanisms of maltol on nephrotoxicity by cisplatin using a cisplatin-treated mouse model and a cellular toxicity model of HEK293 cells. The blood urea nitrogen (BUN), creatinine (CRE) and neutrophil gelatinase-associated lipocalin (NGAL) levels in mice were increased by cisplatin but decreased to normal ranges by maltol pretreatment (50 and 100 mg/kg) for ten days. Besides, maltol pretreatment decreased oxidative stress, lipid peroxidation and apoptosis in cisplatin-treated mice. The inhibitory action of maltol on inflammatory responses was achieved by reducing the expressions in NF-κB, IL-1β, iNOS, and TNF-α in the mice in vivo. Additionally, maltol restored the reduction of PI3K/Akt and mTOR levels by cisplatin through increasing AMPK expression in cisplatin-treated HEK293 cells. Maltol also suppressed the expression of Bax and caspase 3 by inhibiting the p53 activity in HEK293 cells. Overall, maltol may serve as a valuable potential drug to prevent cisplatin-induced nephrotoxicity, and the underlying molecular mechanisms of maltol action may involve intracellular AMPK/PI3K/Akt and p53 signaling pathways.
The Protective Effects of Maltol on Cisplatin-Induced Nephrotoxicity Through the AMPK-mediated PI3K/Akt and p53 Signaling Pathways
Xiao-Jie Mi 1 , Jin-Gang Hou 1 2 , Zi Wang 1 , Ye Han 1 , Shen Ren 1 , Jun-Nan Hu 1 , Chen Chen 3 , Wei Li 4
2018 Oct 29
Maltol, a type of aromatic compound, exists in high concentrations in red ginseng. Maltol is a potent antioxidative agent and typically is used to enhance flavor and preserve food.