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Venkatesh L. Hegde

Researcher at University of South Carolina

Publications -  39
Citations -  1864

Venkatesh L. Hegde is an academic researcher from University of South Carolina. The author has contributed to research in topics: Immune system & Cannabinoid receptor. The author has an hindex of 20, co-authored 34 publications receiving 1577 citations. Previous affiliations of Venkatesh L. Hegde include Central Food Technological Research Institute & Council of Scientific and Industrial Research.

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Cannabinoids as novel anti-inflammatory drugs

TL;DR: This review will focus on the potential use of cannabinoids as a new class of anti-inflammatory agents against a number of inflammatory and autoimmune diseases that are primarily triggered by activated T cells or other cellular immune components.
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Resveratrol (trans-3,5,4'-trihydroxystilbene) ameliorates experimental allergic encephalomyelitis, primarily via induction of apoptosis in T cells involving activation of aryl hydrocarbon receptor and estrogen receptor.

TL;DR: Data from the present study demonstrate the ability of resveratrol to trigger apoptosis in activated T cells and its potential use in the treatment of inflammatory and autoimmune diseases including, MS.
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Attenuation of experimental autoimmune hepatitis by exogenous and endogenous cannabinoids: involvement of regulatory T cells.

TL;DR: The data demonstrate that targeting cannabinoid receptors using exogenous or endogenous cannabinoids and use of FAAH inhibitors may constitute novel therapeutic modalities to treat immune-mediated liver inflammation.
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Role of Myeloid-Derived Suppressor Cells in Amelioration of Experimental Autoimmune Hepatitis Following Activation of TRPV1 Receptors by Cannabidiol

TL;DR: This study demonstrates for the first time that M DSCs play a critical role in attenuating acute inflammation in the liver, and that agents such as CBD, which trigger MDSCs through activation of TRPV1 vanilloid receptors may constitute a novel therapeutic modality to treat inflammatory diseases.
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miR-155 deficiency protects mice from experimental colitis by reducing T helper type 1/type 17 responses

TL;DR: Using an acute experimental colitis model, it is found that miR‐155−/− mice, as compared to wild‐type control mice, have decreased clinical scores, a reversal of colitis‐associated pathogenesis, and reduced systemic and mucosal inflammatory cytokines.