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Abstract
Background/aim: Nutraceuticals have been extensively studied in recent years to find safe therapeutics of natural origin instead of relying only on pharmaceuticals. This study aimed to detect the hepato-protective role of moringa and rosemary ethanolic extracts on liver fibrosis induced by thioacetamide (TAA). Methods: This study was conducted on 60 male albino rats divided into four groups; control, TAA-group (received 100 mg/kg thioacetamide intraperitoneal twice /week for 18 weeks), moringa-protected group (received 300 mg/kg moringa ethanolic extract orally daily with TAA), rosemary-protected group (received 200 mg/kg rosemary ethanolic extract orally daily with TAA for 18 weeks). Results: There were significant increases in liver alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), malondialdehyde (MDA), and nitric oxide (NO) with significant decreases in reduced glutathione (GSH), superoxide dismutase (SOD) in the TAA-treated group with a high degree of fibrosis which extended to cirrhosis after 18 weeks. Meanwhile, both TAA-moringa and TAA-rosemary treated groups showed improvement in biochemical markers and fibrosis induced by TAA. Conclusion: This study proved that both moringa and rosemary could protect the liver against TAA-induced liver fibrosis and rosemary has greater protection than moringa.
Highlights
Liver fibrosis is the result of excessive extracellular matrix (ECM) accumulation (Kisseleva and Brenner, 2011)
This study aimed to detect the hepato-protective role of moringa and rosemary ethanolic extracts on liver fibrosis induced by thioacetamide (TAA)
The addition of moringa or rosemary extract with thioacetamide ameliorated the TAA effect, with significant decreases in the concentrations of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) compared to the TAAtreated group
Summary
Liver fibrosis is the result of excessive extracellular matrix (ECM) accumulation (Kisseleva and Brenner, 2011). Thioacetamide (TAA) is a potent centrilobular hepatotoxic agent which is frequently used in the experimental models of chemically induced hepatotoxicity in rodents. The most common mechanism of action of TAA for cirrhosis induction is the induction of oxidative stress (Helmy et al, 2018). There is no FDA-approved medication for liver fibrosis (Bataller and Brenner, 2005). Many strategies have been conducted to combat liver fibrosis by inhibiting pathways or certain molecular targets that are involved in the development of liver fibrosis. Substantial traditional herbs that possess low adverse effects in the treatment of chronic liver diseases have created considerable interest as protective agents for reducing liver damage (Guo et al, 2013)
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