Several evidences indicate obesity as a risk factor for neurodegenerative diseases. In obesity status insulin signaling is inhibited both in the liver and brain by impairing the signaling cascade at multiple levels and inducing insulin resistance, oxidative stress and inflammation. It has been postulated that cytotoxic ceramides transferred from the liver to the blood can enter the brain due to their lipid-soluble nature, and thereby exert neurodegenerative effects via a liver-brain axis. Thus, using a liver protector supplement, a benefit both for liver and brain should be expected. KEPAR is a commercial natural supplement containing several plant extracts such as turmeric (Curcuma longa), silymarin (Sylibum marianum), guggul (Commiphora mukul), chlorogenic acid (Cynara scolymus), and inulin (Taraxacum officinale) and used for liver protection. C57BL6 mice were fed with a standard diet (STD) or with a high fat diet (HFD), to induce obesity, in absence/presence of KEPAR solution, for 4 mouths. After this treatments the mice were weighted and cholesterol, triglycerides and glucose parameters were measured at baseline to confirm occurrence or inhibition of the metabolic syndrome. After these tests mice were sacrificed and the effect on the brain was analyzed. Brain of mice HFD fed showed an increase of ROS and NO generation that was reduced in mice treated with KEPAR. Western blot analysis suggest that the supplement decrease the levels of HSP60, H- Oxy and i-Nos stress inducted proteins. By immunofluorescence studies we have also demonstrated that the supplement have a anti-inflammatory effect in the brain by decreasing the levels of expression of some inflammatory proteins such as a glial fibrillary acidic protein (GFAP). The neuroprotective role of KEPAR was confirmed by in vitro studies on LAN5 neuroblastoma cells, in which oxidative stress and inflammation was induced and specific markers analyzed.

Effect of a natural liver protector supplement in the brain

D Nuzzo;P Picone;G Galizzi;M Di Carlo
2015

Abstract

Several evidences indicate obesity as a risk factor for neurodegenerative diseases. In obesity status insulin signaling is inhibited both in the liver and brain by impairing the signaling cascade at multiple levels and inducing insulin resistance, oxidative stress and inflammation. It has been postulated that cytotoxic ceramides transferred from the liver to the blood can enter the brain due to their lipid-soluble nature, and thereby exert neurodegenerative effects via a liver-brain axis. Thus, using a liver protector supplement, a benefit both for liver and brain should be expected. KEPAR is a commercial natural supplement containing several plant extracts such as turmeric (Curcuma longa), silymarin (Sylibum marianum), guggul (Commiphora mukul), chlorogenic acid (Cynara scolymus), and inulin (Taraxacum officinale) and used for liver protection. C57BL6 mice were fed with a standard diet (STD) or with a high fat diet (HFD), to induce obesity, in absence/presence of KEPAR solution, for 4 mouths. After this treatments the mice were weighted and cholesterol, triglycerides and glucose parameters were measured at baseline to confirm occurrence or inhibition of the metabolic syndrome. After these tests mice were sacrificed and the effect on the brain was analyzed. Brain of mice HFD fed showed an increase of ROS and NO generation that was reduced in mice treated with KEPAR. Western blot analysis suggest that the supplement decrease the levels of HSP60, H- Oxy and i-Nos stress inducted proteins. By immunofluorescence studies we have also demonstrated that the supplement have a anti-inflammatory effect in the brain by decreasing the levels of expression of some inflammatory proteins such as a glial fibrillary acidic protein (GFAP). The neuroprotective role of KEPAR was confirmed by in vitro studies on LAN5 neuroblastoma cells, in which oxidative stress and inflammation was induced and specific markers analyzed.
2015
Istituto di biomedicina e di immunologia molecolare - IBIM - Sede Palermo
9788890580581
diet supplement
obesity
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/336547
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