30 research outputs found

    The Effects of Morinda citrifolia (Noni) Fruit Juice on the Prevention of Stroke by Promoting Production of Nitric Oxide through the Brain of the Spontaneously Hypertensive Stroke Prone (SHRSP) Rats

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    Morinda citrifolia (Noni) is a traditional folk medicinal plant and has a long history of use as a food and medicine. In order to reveal the effects of Noni fruit juice (NFJ) on stroke prevention, we performed experiments using spontaneously hypertensive stroke prone (SHRSP) rats. NFJ did not change rat body weight, food intake, and water intake. However, both systolic blood pressure (SBP) and diastolic blood pressure (DBP) were significantly decreased after NFJ treatment in SHRSP rats. Furthermore, NFJ significantly increased the survival rate, urinary nitric oxide (NO) concentration was significantly higher in the NFJ group, and endothelial NO synthase (eNOS) phosphorylation levels increased in the brain after NFJ treatment. Two pathways regulate eNOS phosphorylation: the insulin-dependent pathway and the insulin-independent pathway. For the insulin-dependent pathway, phosphorylation of insulin receptor substrate 1 (IRS1) and protein kinase B (Akt) did not change in the NFJ group. For the insulin-independent pathway, expression of adenosine monophosphate-activated protein kinase (AMPK) phosphorylation, liver kinase B 1 (LKB1), and silent information regulator 1 (Sirt1) significantly increased in the brain of SHRSP rats after NFJ treatment. These data suggested that NFJ prevented stroke by improved blood circulation, increased NO production, and elevated eNOS phosphorylation by stimulating the insulin-independent pathway (Sirt1-LKB1-AMPK-eNOS)

    Guava leaf extracts alleviate fatty liver via expression of adiponectin receptors in SHRSP.Z-Leprfa/Izm rats

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    <p>Abstract</p> <p>Background</p> <p>In recent years, the number of people with metabolic syndrome has continued to rise because of changing eating habits, and accompanying hepatic steatosis patients have also increased. This study examined the effect of guava leaf extract on liver fat accumulation using SHRSP.Z-Leprfa/IzmDmcr rats (SHRSP/ZF), which are a metabolic syndrome model animal.</p> <p>Method</p> <p>Seven-week-old male SHRSP/ZF rats were divided into two groups, a control group and a guava leaf extract (GLE) group. We gave 2 g/kg/day GLE or water by forced administration for 6 weeks. After the experimental period, the rats were sacrificed and organ weight, hepatic lipids, serum aminotransferase and liver pathology were examined. To search for a possible mechanism, we examined the changes of key enzyme and transcriptional factors involved in hepatic fatty acid beta-oxidation.</p> <p>Results</p> <p>The triglyceride content of the liver significantly decreased in the GLE group in comparison with the control group, and decreased fat-drop formation in the liver tissue graft in the GLE group was observed. In addition, the improvement of liver organization impairments with fat accumulation restriction was suggested because blood AST and ALT in the GLE group significantly decreased. Furthermore, it was supposed that the activity of AMPK and PPARĪ± significantly increased in the GLE group via the increase of adiponectin receptors. These were thought to be associated with the decrease of the triglyceride content in the liver because AMPK and PPARĪ± in liver tissue control energy metabolism or lipid composition. On the other hand, insulin resistance was suggested to have improved by the fatty liver improvement in GLE.</p> <p>Conclusion</p> <p>Our results indicate that administration of GLE may have preventive effects of hepatic accumulation and ameliorated hepatic insulin resistance by enhancing the adiponectin beta-oxidation system. Guava leaf may be potentially useful for hepatic steatosis without the side effects of long-term treatments.</p

    Guava Leaf Extracts Inhibit 3T3-L1 Adipocyte Differentiation Via Activating AMPK

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    The guava tree (psidium guajava linn.) is commonly used not only as food but also as folk medicine. In our previous studies, we showed that oral administration of guava leaf extracts (GLE) had beneficial anti-obesity effects using metabolic syndrome model rats. However, we did not clarify molecular mechanism by which GLE administration leads to anti-obesity effect. This study was designed to evaluate the mechanism of anti-obesity by GLE using 3T3-L1 pre-adipocyte cell lines. We found that GLE significantly inhibited 3T3-L1 differentiation via down-regulation of adipogenic transcription factors and markers. Mitotic clonal expansion, which is essential for adipose differentiation, was also depressed in the early phase. Interestingly, GLE increased the phosphorylation of AMPK on 3T3-L1 cells and, by pretreatment with AMPK siRNA, the GLE treatment group showed restored adipocyte differentiation. In conclusion, these results showed that GLE is capable of inhibiting adipocyte differentiation via AMPK activation and therefore it may prevent obesity in vivo

    Beneficial effect of Sparassis crispa on stroke through activation of Akt/eNOS pathway in brain of SHRSP

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    Sparassis crispa (S. crispa) is a mushroom used as a natural medicine that recently became cultivatable in Japan. In this study, we investigated not only the preventive effects of S. crispa against stroke and hypertension in stroke-prone spontaneously hypertensive rats (SHRSP) but also the mechanism involved by using studies of the cerebral cortex at a young age. Six-week-old male SHRSP were divided into 2 groups, a control group and an S. crispa group administered 1.5% S. crispa in feed, and we then observed their survival. In addition, rats of the same age were treated with 1.5% S. crispa for 4Ā weeks and we measured body weight, blood pressure, blood flow from the tail, NOx production, and the levels of expression of several proteins in the cerebral cortex by western blot analysis. Our results showed that the S. crispa group had a delayed incidence of stroke and death and significantly decreased blood pressure and increased blood flow after the administration. Moreover, the quantity of urinary excretion and the nitrate/nitrite concentration in cerebral tissue were higher than those of control SHRSP rats. In the cerebral cortex, phosphor-eNOS (Ser1177) and phosphor-Akt (Ser473) in S. crispa-treated SHRSP were increased compared with those of control SHRSP rats. In conclusion, S. crispa could ameliorate cerebrovascular endothelial dysfunction by promoting recovery of Akt-dependent eNOS phosphorylation and increasing NO production in the cerebral cortex. S. crispa may be useful for preventing stroke and hypertension

    Inhibitory Effect of Buah Merah Oil on Melanogenesis Via Degradation of Tyrosinase

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    Buah Merah (Pandanus conoideus) is exclusively distributed in Papua island and its neighboring areas. The extract oil from fruits (Buah Merah oil) contains rich in lipids, carotenoids and vitamin E.We assessed the effects of Buah Merah oil on melanogenesis in B16 melanoma cells. In the presence of alpha-melanocyte stimulating hormone (Ī±-MSH), B16 melanoma cells are stimulated to enhance melanin synthesis. Buah Merah oil inhibited Ī±-MSH-induced melanin synthesis with no cytotoxicity. This decrease in melanogenesis was correlated with reduced enzyme activity and decreased protein expression levels of tyrosinase. Tyrosinase is a type 1 membrane glycoprotein that is the critical rate-limiting enzyme involved in melanin synthesis. Furthermore, the Buah Merah oil-induced decrease in melanin content was accompanied by a decrease in the amount and activity of tyrosinase whereas the mRNA level of tyrosinase was unchanged. Moreover, treatment with proteasome inhibitor MG132 blocked the down-regulation of melanogenesis by Buah Merah oil. Immunoprecipitation analysis also revealed that treatment with Buah Merah oil modulated the ubiquitination of tyrosinase, that is Buah Merah oil increased the amount of ubiquitinated tyrosinase.Taken together, the present results indicate that the depigmenting effect of Buah Merah oil might be due to inhibition of tyrosinase expression through the ubiquitin proteasome-mediated degradation of tyrosinase
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