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Venkatesan, Ramu,Shim, Won-Sik,Yeo, Eui-Ju,Kim, Sun Yeou Elsevier Ireland Ltd 2017 Journal of Ethnopharmacology Vol.198 No.-
<P><B>Abstract</B></P> <P><B>Ethno-pharmacological relevance</B></P> <P>Lactucopicrin is one of constitutes in <I>Cichorium intybus L,</I> which is commonly known as chicory in worldwide. It has been used for traditional usage such as antianalgesics, antidepressants and antihyperglycemics</P> <P><B>Aim of study</B></P> <P>We investigated the neurotrophin-mediated neuroprotective effect of lactucopicrin in <I>in vitro</I> and examined for the underlying mechanism.</P> <P><B>Materials and method</B></P> <P>To verify the neuroprotective effect of lactucopicrin, we investigated the inhibitory AChE activity, neurite outgrowth-related downstream signaling in murine neuroblastoma N2a and neurotrophins secretion in rat C6 glioma cells.</P> <P><B>Results</B></P> <P>Lactucopicrin inhibited the AChE activity and increased intracellular Ca<SUP>2+</SUP> levels with a substantial rise in muscarinic acetylcholine receptor M1 (CHRM1) expression in N2a cells. Moreover, lactucopicrin actively promoted neurite outgrowth via Ca<SUP>2+</SUP>-mediated activation of Ca<SUP>2+</SUP>/calmodulin-dependent protein kinase-II (CaMKII). It further activates transcription factor 1 (ATF1) along with modulating the levels of tropomyosin receptor kinase A, extracellular signal-regulated kinase 1 and 2, AKT, and synaptophysin 1 in N2a cells. Additionally, the levels of neurotrophins including NGF, BDNF, and NT3 were increased by treatment of lactucopicrin in C6 cells. The effects of lactucopicrin on NGF secretion and neuritogenesis were maintained even in the presence of phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002, indicating that lactucopicrin exerts its effect on neuritogenesis in a PI3K-independent manner.</P> <P><B>Conclusion</B></P> <P>Our results suggest that the natural compound lactucopicrin may be a promising neurotrophin-mediated neuroprotective candidate for neurodegenerative diseases.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Venkatesan, Ramu,Ji, Eunhee,Kim, Sun Yeou Hindawi Publishing Corporation 2015 BioMed research international Vol.2015 No.-
<P>Alzheimer's disease (AD), characterized by progressive dementia and deterioration of cognitive function, is an unsolved social and medical problem. Age, nutrition, and toxins are the most common causes of AD. However, currently no credible treatment is available for AD. Traditional herbs and phytochemicals may delay its onset and slow its progression and also allow recovery by targeting multiple pathological causes by antioxidative, anti-inflammatory, and antiamyloidogenic properties. They also regulate mitochondrial stress, apoptotic factors, free radical scavenging system, and neurotrophic factors. Neurotrophins such as BDNF, NGF, NT3, and NT4/5 play a vital role in neuronal and nonneuronal responses to AD. Neurotrophins depletion accelerates the progression of AD and therefore, replacing such neurotrophins may be a potential treatment for neurodegenerative disease. Here, we review the phytochemicals that mediate the signaling pathways involved in neuroprotection specifically neurotrophin-mediated activation of Trk receptors and members of p75<SUP>NTR</SUP> superfamily. We focus on representative phenolic derivatives, iridoid glycosides, terpenoids, alkaloids, and steroidal saponins as regulators of neurotrophin-mediated neuroprotection. Although these phytochemicals have attracted attention owing to their <I>in vitro</I> neurotrophin potentiating activity, their <I>in vivo</I> and clinical efficacy trials has yet to be established. Therefore, further research is necessary to prove the neuroprotective effects in preclinical models and in humans. </P>
권오욱,Ramu Venkatesan,도문호,지은희,조동운,이기원,김선여 한국식품과학회 2015 Food Science and Biotechnology Vol.24 No.2
This study evaluated the protective effects of dietary supplementation with a fermented barley and soybean mixture (BS) on ultraviolet (UV) B-induced photoaging in hairless mice. Skin aging-related parameters and protein levels related to skin wrinkles and moisturization in mice were analyzed. The BS reduced wrinkle formation, skin thickening, transepidermal water loss, and matrix metalloproteinases- 1 expression in skin. Skin hydration and pH were increased in the BS group. BS attenuated filaggrin expression as well as free amino acid and glycerol production. BS increased superoxide dismutase activity as well as increased expression of nuclear factor (erythroidderived 2)-like 2, procollagen type-I, and decreased erythema. These results suggest that BS protects against photoaging induced by UVB in vivo, indicating the potential of such mixtures as anti-photoaging dietary supplementation.
Subedi, Lalita,Venkatesan, Ramu,Kim, Sun Yeou MDPI 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.7
<P>Allyl isothiocyanate (AITC), present in <I>Wasabia japonica</I> (wasabi), is an aliphatic isothiocyanate derived from the precursor sinigrin, which is a glucosinolate present in vegetables of the Brassica family. Traditionally, it has been used to treat rheumatic arthralgia, blood circulation, and pain. This study focuses on its anti-apoptotic activity through the regulation of lipopolysaccharide (LPS)-induced neuroinflammation. Furthermore, we assessed its neuroprotective efficacy, which it achieves through the upregulation of nerve growth factor (NGF) production. Pretreatment with AITC significantly inhibited inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression, decreased tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), prostaglandin E2 (PGE2), and nitric oxide (NO) production in activated microglia, and increased the nerve growth factor (NGF) and neurite outgrowth in neuroblastoma cells. AITC inhibited the nuclear factor (NF-κB-mediated transcription by modulating mitogen activated protein kinase (MAPK) signaling, particularly downregulating c-Jun N-terminal kinase (JNK) phosphorylation, which was followed by a reduction in the TNF-α expression in activated microglia. This promising effect of AITC in controlling JNK/NF-κB/TNF-α cross-linking maintains the <I>Bcl-2</I> gene family and protects neuroblastoma cells from activated microglia-induced toxicity. These findings provide novel insights into the anti-neuroinflammatory effects of AITC on microglial cells, which may have clinical significance in neurodegeneration.</P>