Metabolomic Profiling of Sansevieria trifasciata hort ex. Prain Leaves and Roots by HPLC-PAD-ESI/MS and its Hepatoprotective Effect via Activation of the NRF2/ARE Signaling Pathway in an Experimentally Induced Liver Fibrosis Rat Model

Document Type : Original Article


1 Pharmacognosy Department, National Research Centre, Dokki, 12622 Giza, Egypt

2 Pharmacology dep., National Research centre

3 Pharmacology Department, National Research Centre, Giza 12622, Egypt

4 Department of Chemistry, College of Science, King Khalid University, Abha 61421, Saudi Arabia Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Cairo University, Giza 12211, Egypt

5 Natural Compounds Chemistry Department, National Research Centre, Dokki, Giza, Egypt


Sansevieria species show various bioactivities. Nevertheless, its therapeutic prospect in liver fibrosis even now is uninvestigated. The present study was conducted to analyze the metabolomic profile of Sansevieria trifasciata hort ex. Prain leaves and roots via HPLC-PAD-ESI/MS and evaluation of its hepatoprotective effect. The identified phytoconstituents were mainly steroidal saponins, phenolics and terpenoids. Sixty-one compounds were tentatively identified in StLE and fifty-nine compounds in StRE. Thioacetamide-induced liver fibrosis rat model was used to evaluate the hepatoprotective effect of Sansevieria trifasciata extracts via activation of the NRF2/ARE signaling pathway. Measurements of serum alanine transaminase (ALT), aspartate transaminase (AST) and malondialdehyde (MDA) were significantly decreased in treated groups with StLE and StRE (at doses of 200 and 100 mg/kg/day) compared with the TAA group. Also, the levels of reduced glutathione (GSH) content and hepatic mRNA levels of Nrf2, HO-1, NQO-1 and Keap-1 were markedly elevated. The prominent hepatoprotective effect was shown in StRE treated groups. Histological findings further confirmed the protective role of the plant against TAA-induced liver fibrosis. In conclusion, the abovementioned results indicated that the hepatoprotective mechanism of StLE and StRE could be achieved by activating Nrf2-ARE signaling pathways to alleviate oxidative stress and inflammation.


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