Maslinic Acid Reduces Blood Glucose in KK-Ay Mice

Liu, Jun; Sun, Hongbin; Duan, Weigang; Mu, Dongyan; Zhang, Luyong

doi:10.1248/bpb.30.2075

Cited by 94 publications

(67 citation statements)

References 16 publications

(10 reference statements)

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“…1,2 MA (2a,3b-2,3-dihydroxy-olean-12-en-28-oic acid), which is abundant in olive fruit skin, has attracted much attention due to its anti-tumor, 3 anti-HIV, 4 anti-oxidation 5 and hypoglycemic [6][7][8] activities. However, important questions whether MA can prevent oxidative stress to consequently alleviate or ameliorate microvascular and macrovascular complications in diabetes remain unanswered.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant effects of maslinic acid in livers, hearts and kidneys of streptozotocin-induced diabetic rats: effects on kidney function

et al. 2013

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Studies indicate that hyperglycemia-induced oxidative stress triggers the development of microvascular and macrovascular complications in diabetes. Accordingly, we hypothesized that maslinic acid (MA) prevents these complications due to its antioxidant properties. We, therefore, investigated the effects of 5-week MA treatment of streptozotocin (STZ)-induced diabetic rats on anti-oxidative status of cardiac, hepatic and renal tissues as well as on kidney function. Proximal tubular effects of MA were studied in anesthetized rats challenged with hypotonic saline after a 3.5 h equilibration for 4 h of 1 h control, 1.5 h treatment and 1.5 h recovery periods using lithium clearance. MA was added to the infusate during the treatment period. Oral glucose tolerance responses to MA were monitored in rats given a glucose load after an 18 h fast. Compared with untreated diabetic rats, MA-treated diabetic animals exhibited significantly low malondialdehyde (MDA, a marker of lipid peroxidation) and increased the activity of antioxidant enzymes; superoxide dismutase and glutathione peroxidase in hepatic, cardiac and renal tissues. The expressions of gastrocnemius muscle GLUT4 and kidney GLUT1 and GLUT2 were assessed to elucidate the mechanism of the hypoglycemic effects of MA. MA-treatment diminished the expression of GLUT1 and GLUT2 in diabetic kidney and reduced glycemia values of diabetic rats. MA administration increased urinary Na þ outputs and additionally the FE Na indicating that at least part of the overall reduction in Na þ reabsorption occurred in the proximal tubules. These results suggest antioxidant effects of MA can ameliorate oxidative stress and improve kidney function in diabetes mellitus.

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Section: Introductionmentioning

confidence: 99%

Antioxidant effects of maslinic acid in livers, hearts and kidneys of streptozotocin-induced diabetic rats: effects on kidney function

et al. 2013

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“…Maslinic acid (MA), a pentacyclic triterpene acid, is widely present in dietary plants, especially abundant in olive fruit skins and hawthorn. The compound has attracted much interest owing to its proven pharmacologic safety and its many biologic activities, such as anti-inflammatory, (2) antiviral, (3) antioxidant, (2,4) and antidiabetogenic activities (5,6) and anti-colon cancer (7) and antiastrocytoma (8) properties. In this study we examined the effects of MA on osteoclast differentiation and function in vitro and in vivo and then elucidated the underlying molecular mechanisms.…”

mentioning

confidence: 99%

Maslinic acid suppresses osteoclastogenesis and prevents ovariectomy-induced bone loss by regulating RANKL-mediated NF-κB and MAPK signaling pathways

Yang

et al. 2010

Journal of Bone and Mineral Research

117

100

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Activation of NF-kB and MAPK/activator protein 1 (AP-1) signaling pathways by receptor activator NF-kB ligand (RANKL) is essential for osteoclast activity. Targeting NF-kB and MAPK/AP-1 signaling to modulate osteoclast activity has been a promising strategy for osteoclast-related diseases. In this study we examined the effects of maslinic acid (MA), a pentacyclic triterpene acid that is widely present in dietary plants, on RANKL-induced osteoclastogenesis, osteoclast function, and signaling pathways by in vitro and in vivo assay systems. In mouse bone marrow monocytes (BMMs) and RAW264.7 cells, MA inhibited RANKL-induced osteoclastogenesis in a dosedependent manner within nongrowth inhibitory concentration, and MA decreased osteoclastogenesis-related marker gene expression, including TRACP, MMP9, c-Src, CTR, and cathepsin K. Specifically, MA suppressed osteoclastogenesis and actin ring formation at early stage. In ovariectomized mice, administration of MA prevented ovariectomy-induced bone loss by inhibiting osteoclast activity. At molecular levels, MA abrogated the phosphorylation of MAPKs and AP-1 activity, inhibited the IkBa phosphorylation and degradation, blocked NF-kB/p65 phosphorylation, nuclear translocation, and DNA-binding activity by downregulating RANK expression and blocking RANK interaction with TRAF6. Together our data demonstrate that MA suppresses RANKL-induced osteoclastogenesis through NF-kB and MAPK/AP-1 signaling pathways and that MA is a promising agent in the treatment of osteoclast-related diseases such as osteoporosis. ß

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“…There are a lot of theories about the pathogenesis of atherosclerosis, one of which is abnormal cholesterol levels [53]. The flavone extracted from C. pinnatifida by 70% ethanol obviously decreased the serum levels of total cholesterol (TC), triglyceride and low-density lipoprotein cholesterol (LDLC) in high-fat/cholesterol rabbit and rat models, suggesting its use to treat atherosclerosis [54].…”

Section: Lipid Regulating and Anti-atherosclerosis Effectsmentioning

confidence: 99%

Crataegus pinnatifida: Chemical Constituents, Pharmacology, and Potential Applications

et al. 2014

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Abstract:Crataegus pinnatifida (Hawthorn) is widely distributed in China and has a long history of use as a traditional medicine. The fruit of C. pinnatifida has been used for the treatment of cardiodynia, hernia, dyspepsia, postpartum blood stasis, and hemafecia and thus increasing interest in this plant has emerged in recent years. Between 1966 and 2013, numerous articles have been published on the chemical constituents, pharmacology or pharmacologic effects and toxicology of C. pinnatifida. To review the pharmacologic advances and to discuss the potential perspective for future investigation, we have summarized the main literature findings of these publications. So far, over 150 compounds including flavonoids, triterpenoids, steroids, monoterpenoids, sesquiterpenoids, lignans, hydroxycinnamic acids, organic acids and nitrogen-containing compounds have been isolated and identified from C. pinnatifida. It has been found that these constituents and extracts of C. pinnatifida have broad pharmacological effects with low toxicity on, for example, the cardiovascular, digestive, and endocrine systems, and pathogenic microorganisms, supporting the view that C. pinnatifida has favorable therapeutic effects. Thus, although C. pinnatifida has already been widely used as pharmacological therapy, due to its various active compounds, further research is warranted to develop new drugs.

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Maslinic Acid Reduces Blood Glucose in KK-Ay Mice

Cited by 94 publications

References 16 publications

Antioxidant effects of maslinic acid in livers, hearts and kidneys of streptozotocin-induced diabetic rats: effects on kidney function

Antioxidant effects of maslinic acid in livers, hearts and kidneys of streptozotocin-induced diabetic rats: effects on kidney function

Maslinic acid suppresses osteoclastogenesis and prevents ovariectomy-induced bone loss by regulating RANKL-mediated NF-κB and MAPK signaling pathways

Crataegus pinnatifida: Chemical Constituents, Pharmacology, and Potential Applications

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