From: Promising hepatoprotective agents from the natural sources: a study of scientific evidence
S.no | Modern medicine | Disease condition | Mechanism of action | Clinical outcomes | Reference |
---|---|---|---|---|---|
1 | Corticosteroids | Reduce cytokine production Antifibrotic | Switch off multiple activated inflammatory genes through inhibition of histone acetyltransferase (HAT) and recruitment of histone deacetylase 2 (HDAC2) activity to the inflammatory gene transcription complex | Studies revealed that it has less significant effect nowadays, and implication in future as liver-protective agent is also less recognized | |
2 | Interferons | Antiviral, antifibrotic | Inhibits hepatitis B and C virus replication by decreasing RNA transcription, occurring from covalently closed circular DNA | Hepatitis B and C could be treated. Antifibrotic activity is still not tested and proved in human. Side effects at therapeutic dose include depression, anxiety, agitation, suicidal ideation, and even suicide | |
3 | Lamivudine | Hepatitis B and cirrhosis | Converted intracellularly to its triphosphate form which then competes with cytosine triphosphate for incorporation into the developing viral DNA strand | Continuous usage might result in the development of resistant with hepatitis B virus | |
4 | Propylthiouracil | Alcohol hepatic diseases | Reacts with some of the oxidizing species derived from the respiratory burst in neutrophils and act as antioxidant resulting in the suppression of alcohol-induced hepatic necrosis | Render metabolically compromised patients hypothyroid | |
5 | Colchicine | Against gout, antifibrotic | Disrupts tubulin leading to subsequent downregulation of multiple inflammatory pathways and modulation of innate immunity | Beneficial properties were not demonstrated recently. Very toxic at high doses | |
6 | Pentoxifylline | Severe alcoholic hepatitis | Inhibits TNF-alpha synthesis and inflammation | Have appropriate therapeutic implication for hepatorenal syndrome due to its excellent safety profile. Patients with xanthine hypersensitivity should avoid use of pentoxifylline | [111] |
7 | Ursodeoxycholic acid | Non-alcoholic fatty hepatic disease | Inhibits DNA repair, coenzyme A, cyclic AMP, p53, and phagocytosis and inhibits induction of nitric oxide synthetase | Useful in the treatment of hepatobiliary diseases by ameliorating hepatic histology, enzymes, and different oxidative stress Long use of ursodeoxycholic acid in human might result in taurine depletion | |
8 | Rosiglitazone | Non-alcoholic fatty hepatic disease | Activates intracellular receptor class of peroxisome proliferator-activated receptors (PPARs), specifically PPARγ | Increase risk of heart attack |