The liver is in charge of a wide range of critical physiological processes and it plays an important role in activating the innate immune system which elicits the inflammatory events. Chronic ethanol exposure disrupts hepatic inflammatory mechanism and leads to the release of proinflammatory mediators such as chemokines, cytokines and activation of inflammasomes. The mechanism of liver fibrosis/cirrhosis involve activation of NLRP3 inflammasome, leading to the destruction of hepatocytes and subsequent metabolic dysregulation in humans. In addition, increasing evidence suggests that alcohol intake significantly modifies liver epigenetics, promoting the development of alcoholic liver disease (ALD). Epigenetic changes including histone modification, microRNA-induced genetic modulation, and DNA methylation are crucial in alcohol-evoked cell signaling that affects gene expression in the hepatic system. Though we are at the beginning stage without having the entire print of epigenetic signature, it is time to focus more on NLRP3 inflammasome and epigenetic modifications. Here we review the novel aspect of ALD pathology linking to inflammation and highlighting the role of epigenetic modification associated with NLRP3 inflammasome and how it could be a therapeutic target in ALD.

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Coccinia indica is a vine that majorly grows in tropical climates. It is commonly used in south Asian cuisine and is known to show various medicinal properties. Various parts of the plant are used as a medicine such as roots, fruits and leaves. It is commonly known to cure disease such as liver disease, asthma, ulcer, urinary infection, allergy, bronchitis. In the current study, we try to understand the hepatoprotective and anti-arthritis of the plant via insilico docking methodologies. Firstly, the plant extract was subjected to GCMS analysis and the active components of the plant were obtained. The most reactive compounds amongst the result were chosen as ligands to conduct in-silico docking against the receptors of hepatoxicity and arthritis. Ligands like Pterin-6-carboxylic acid, 2r,3s-9-[[1,3-Dihydroxy-4-Fluoro-3-Butoxy]Methyl]Gu, D(17a)-Homo-C,18-dinorcard-20(22)-enolide, 14hydroxy-17a-methylene-3-oxo-, (5.beta.) -Showed potential interaction against chosen receptors. Coccinia indica active compound has shown better binding affinity between hepatotoxicity and arthritis receptors. The potential active compound of Coccinia indica can be further studied in animal models to demonstrate its beneficial activities.

Acute pancreatitis (AP) being one of the rapidly emerging gastrointestinal concerns, needs early surveillance as the instantaneous inflammatory response in the pancreas may lead to severe pathological clinical phenotypes. Failure in monitoring AP may lead to severe inflammatory response syndrome (SIRS) which is seen amongst one-fifth of individuals requiring extensive management and palliative care to prevent the disease progression. However, the major question of defining a definitive pool of molecular targets for AP remains unanswered thus far. As a first step towards designing a definitive pool of molecular targets for AP, we aim to compile the reported evidence of potential signaling molecules in AP. During AP, the inflammatory response-inducing factors trigger multiple signaling molecules that cause the pancreatic tissue assault. As a counter-active response, the host body's immune system initiates the resolution of inflammation and repair of the damaged tissue by stimulating various anti-inflammatory signaling molecules. The communication between the components of these pro-inflammatory and anti-inflammatory signaling pathways opens up a wide window for the identification of various prognostic markers and molecular targets for the management of AP. This review collectively presents the available prognostic biomarkers in detail for a better prognosis of AP.