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Anti?inflammatory compounds moracin O and P from Morus alba Linn. (Sohakuhi) target the NF??B pathway.

ABSTRACT: Accumulating evidence suggests that inflammation is linked to multiple pathological processes and induces cellular and molecular damage through the activation of inflammatory signaling pathways, including the NF??B pathway. The aim of the present study was to identify natural anti?inflammatory products that can target NF??B activity, in order to establish a novel therapeutic approach for inflammatory diseases. Using a 4T1 breast cancer cell line that expresses the firefly luciferase gene under the control of an NF??B response element, 112 natural products were tested for their anti?inflammatory properties. Sohakuhi (Morus alba Linn. bark) extract was observed to strongly suppress NF??B activity without affecting cell viability. To further examine the anti?inflammatory effect of Sohakuhi, tumor necrosis factor?related apoptosis?inducing ligand (TRAIL)?induced cellular damage of human HaCaT keratinocytes was evaluated. While TRAIL triggered the phosphorylation of the p65 subunit of NF??B, leading to cellular damage in HaCaT cells, treatment with Sohakuhi extract protected HaCaT cells against TRAIL?induced cellular damage. Moreover, Sohakuhi treatment also upregulated the anti?apoptotic proteins Bcl?xL and Bcl?2. Importantly, through chemical fractionation of Sohakuhi extract, moracin O and P were confirmed to mediate its anti?inflammatory effects. Collectively, the present results indicated that Sohakuhi and moracin may represent potential candidates for the development of novel anti?inflammatory drugs.

SUBMITTER: Hardianti B

PROVIDER: S-EPMC7647032 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Anti‑inflammatory compounds moracin O and P from Morus alba Linn. (Sohakuhi) target the NF‑κB pathway.

Hardianti Besse B Umeyama Lin L Li Feng F Yokoyama Satoru S Hayakawa Yoshihiro Y

Molecular medicine reports 20201020 6

Accumulating evidence suggests that inflammation is linked to multiple pathological processes and induces cellular and molecular damage through the activation of inflammatory signaling pathways, including the NF‑κB pathway. The aim of the present study was to identify natural anti‑inflammatory products that can target NF‑κB activity, in order to establish a novel therapeutic approach for inflammatory diseases. Using a 4T1 breast cancer cell line that expresses the firefly luciferase gene under t ...[more]

PMID: 33173971

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Project description:Elevations in plasma levels of pro-inflammatory cytokines and C-reactive protein (CRP) in patient blood have been associated with impairments in cognitive abilities and more severe psychiatric symptoms in people with schizophrenia. The transcription factor nuclear factor kappa B (NF-κB) regulates the gene expression of pro-inflammatory factors whose protein products trigger CRP release. NF-κB activation pathway mRNAs are increased in the brain in schizophrenia and are strongly related to neuroinflammation. Thus, it is likely that this central immune regulator is also dysregulated in the blood and associated with cytokine and CRP levels. We measured levels of six pro-inflammatory cytokine mRNAs and 18 mRNAs encoding NF-κB pathway members in peripheral blood leukocytes from 87 people with schizophrenia and 83 healthy control subjects. We then assessed the relationships between the alterations in NF-κB pathway genes, pro-inflammatory cytokine and CRP levels, psychiatric symptoms and cognition in people with schizophrenia. IL-1β and IFN-γ mRNAs were increased in patients compared to controls (both p < 0.001), while IL-6, IL-8, IL-18, and TNF-α mRNAs did not differ. Recursive two-step cluster analysis revealed that high levels of IL-1β mRNA and high levels of plasma CRP defined 'high inflammation' individuals in our cohort, and a higher proportion of people with schizophrenia were identified as displaying 'high inflammation' compared to controls using this method (p = 0.03). Overall, leukocyte expression of the NF-κB-activating receptors, TLR4 and TNFR2, and the NF-κB subunit, RelB, was increased in people with schizophrenia compared to healthy control subjects (all p < 0.01), while NF-κB-inducing kinase mRNAs IKKβ and NIK were downregulated in patients (all p < 0.05). We found that elevations in TLR4 and RelB appear more related to inflammatory status than to a diagnosis of schizophrenia, but changes in TNFR2 occur in both the high and low inflammation patients (but were exaggerated in high inflammation patients). Further, decreased leukocyte expression of IKKβ and NIK mRNAs was unique to high inflammation patients, which may represent schizophrenia-specific dysregulation of NF-κB that gives rise to peripheral inflammation in a subset of patients.

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Anti?inflammatory compounds moracin O and P from Morus alba Linn. (Sohakuhi) target the NF??B pathway.

Publications

Anti‑inflammatory compounds moracin O and P from Morus alba Linn. (Sohakuhi) target the NF‑κB pathway.

Similar Datasets

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