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Tender coconut water suppresses hepatic inflammation by activating AKT and JNK signaling pathways in an in vitro model of sepsis.

ABSTRACT: Tender coconut water (TCW) is a natural plant product rich in phytochemicals and protects against toxic liver injury. However, the mechanism by which TCW inhibits inflammation and tissue damage is unknown. We examined the effect of TCW on primary rat hepatocyte viability, cytokine-induced gene expression and proinflammatory signaling in an in vitro model of sepsis. We observed that TCW improved hepatocyte viability and protected hepatocytes against cytokine-mediated cell death. TCW suppressed IL-1?-mediated increases in Nos2, Tnf, and Il6 mRNA and increased heme oxygenase 1 (HMOX1) protein. TCW inhibited iNOS expression through activation of AKT and JNK pathways since inhibition of PI3K and JNK signaling reduced TCW's effect on iNOS protein expression and activity. These results demonstrate that TCW reduces proinflammatory gene expression and hepatocyte injury produced by elevated inflammatory cytokines and nitric oxide production.

SUBMITTER: Lakshmanan J

PROVIDER: S-EPMC7449535 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Tender coconut water suppresses hepatic inflammation by activating AKT and JNK signaling pathways in an <i>in vitro</i> model of sepsis.

Lakshmanan Jaganathan J Zhang Baochun B Wright Kalen K Motameni Amierreza T AT Jaganathan Vaitheesh V Schultz David J DJ Klinge Carolyn M CM Harbrecht Brian G BG

Journal of functional foods 20191031

Tender coconut water (TCW) is a natural plant product rich in phytochemicals and protects against toxic liver injury. However, the mechanism by which TCW inhibits inflammation and tissue damage is unknown. We examined the effect of TCW on primary rat hepatocyte viability, cytokine-induced gene expression and proinflammatory signaling in an <i>in vitro</i> model of sepsis. We observed that TCW improved hepatocyte viability and protected hepatocytes against cytokine-mediated cell death. TCW suppre ...[more]

PMID: 32863888

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Project description:The investigation was aimed to understand the effect of coconut milk, tender coconut pulp, tender coconut water and coconut sugar on the qualitative attributes of ice cream. Five ice cream formulations were laid out to substitute the major ingredients of ice cream such as, dairy milk and butter with coconut milk, skim milk powder with tender coconut pulp, refined sugar with coconut sugar and potable water with tender coconut water. Two of the formulations were exclusively non-dairy, third one was the standard dairy ice cream, fourth formulation was with the inclusion of coconut sugar in the standard ice cream and the fifth one was standard ice cream with tender coconut and coconut sugar. Proximate composition of the raw materials revealed that coconut milk, tender coconut pulp and coconut sugar can contribute to the solids-non-fat content in ice cream. Significant effect (p< 0.01) was observed on physico-chemical qualities of the mix and ice cream. Total solids, density and total soluble solids of the ice cream mixes were positively correlated. Density, one of the key physical parameters was ranged from 0.98 to 1.13 g/ cm3. Though coconut milk is acidic, the percent titratable values were within the limit. Non- dairy ice cream formulations obtained lower overrun (p < 0.001). There was a negative correlation between percent fat of ice cream and overrun. Crude fat and protein contents of the ice creams were ranged from 10.52-11.62 % and 3.42-4.94 % respectively. Inclusion of coconut products resulted in increased total phenolics and minerals (ash). Non-dairy formulations were preferred over dairy counterpart with respect to flavour and taste during the sensory evaluation carried out with four different age groups. Thus, the study enlightens the potential scope of utilization coconut products in ice cream industry. It also gave a lead towards developing non-dairy/ vegan delicacy on coconut.Supplementary informationThe online version contains supplementary material available at 10.1007/s13197-021-05279-y.

Project description:BackgroundBMP3 gene is often found hypermethylated and hence inactivated in several types of cancers including colorectal cancer (CRC), indicating that it has a suppressor role in carcinogenesis. Though BMP3 is a reliable biomarker for screening CRC, the molecular mechanism of BMP3 in carcinogenesis remains largely unknown.MethodsThe expression level of BMP3 was examined by immunohistochemistry staining and western blot. Methylation-specific PCR (MSP) and real-time quantitative MSP were used to test the hypermethylation status of BMP3 gene. Analyses of BMP3 function in colon cancer cell proliferation, migration, invasion, and apoptosis were performed using HCT116 and KM12 cells. BMP3 was further knocked down or overexpressed in CRC cells, and the effects on cell growth of xenograft tumors in nude mice were assessed. Co-immunoprecipitation and immunofluorescence staining were used to analyze the association between BMP3 and BMPR2 or BMP3 and ActRIIB. Microarray analysis was performed to identify most differentially expressed genes and pathways regulated by BMP3. The BMP3-regulated SMAD2-dependent signaling pathway and TAK1/JNK signal axes were further investigated by quantitative PCR and western blot.ResultsBMP3 gene was hypermethylated and its expression was downregulated in both CRC tissues and cell lines. Expressing exogenous BMP3 in HCT116 inhibited cell growth, migration, and invasion and increased rate of apoptosis both in vitro and in vivo. However, shRNA-mediated attenuation of endogenous BMP3 in KM12 reversed such inhibitory and apoptotic effects. Furthermore, BMP3 could bind to ActRIIB, an activin type II receptor at the cellular membrane, thereby activating SMAD2-dependent pathway and TAK1/JNK signal axes to regulate downstream targets including caspase-7, p21, and SMAD4 that play crucial roles in cell cycle control and apoptosis.ConclusionsOur study reveals a previously unknown mechanism of BMP3 tumor suppression in CRC and provides a rationale for future investigation of BMP3 as a potential target for the development of novel therapeutic agents to fight CRC.

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Tender coconut water suppresses hepatic inflammation by activating AKT and JNK signaling pathways in an in vitro model of sepsis.

Publications

Tender coconut water suppresses hepatic inflammation by activating AKT and JNK signaling pathways in an <i>in vitro</i> model of sepsis.

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