Phytochemical Profiling, Acute Toxicity, and Hepatoprotective Effects of Anchusa Limbata in Thioacetamide‐Induced Liver Cirrhosis in Rats

ABSTRACT Evaluation of Anchusa species of the family Boraginaceae during previous investigations determined numerous therapeutic potentials against inflammatory‐related diseases. The present study evaluates the phytochemical, acute toxicity, and hepatoprotective effects of methanolic extracts of Anchusa limbata (MEAL) against thioacetamide (TAA)‐induced liver injury in rats. The phytochemical profiling of MEAL followed a Folin–Ciocalteu and 10% AlCl3 procedure using a spectrophotometer. Thirty rats were divided into 5 groups: Normal (A) and TAA control rats (B) treated orally with daily 10% tween 20; reference rats (C) received daily oral dose of 50 mg/kg silymarin; (D and E) rats received daily doses of 250 and 500 mg/kg MEAL, respectively. In addition, group B‐E received 3 injections of 200 mg/kg TAA weekly for 60 days. The phytochemical profiling showed increased polyphenolic (129.2 mg gallic acid equivalent/g) and flavonoid (105.3 mg quercetin equivalent/g extract) contents in MEAL. The TAA intraperitoneal injection caused significant hepatic dysfunctionality (lowered total protein, 54.7 g/L; albumin levels, 7.8 g/L), hepatotoxicity, and necrotized cell proliferation. TAA hepatotoxicity resulted in an increased expression of proliferating cell nuclear antigen (PCNA), TGF‐β1 tissue expression, liver enzymatic leakage, and oxidative stress biomarkers, while it reduced pro‐apoptotic Bcl‐2–associated X protein (Bax) proteins and inflammatory mediators (TNF‐α and IL‐6) and increased IL‐10. Conversely, MEAL treatment ameliorated the TAA‐induced hepatotoxicity and restored liver functions. The present hepatoprotectives of MEAL could be attributed to its increased polyphenolic and flavonoid contents, which require further isolation and identification of molecules underlying such therapeutic actions. The phytochemical profiling showed increased polyphenolic (129.2 mg GAE/g) and flavonoid (105.3 mg EQ/g extract) contents in methanolic extract of Anchusa limbata. The present of MEAL supplementation ameliorated TAA‐mediated hepatoxicity in rats by modulating several molecular mechanisms. MEAL oral ingestion reduced expression of proliferating cell nuclear antigen (PCNA), TGF‐β1 tissue expression, liver enzymatic leakage, and oxidative stress biomarkers, while it up‐regulated pro‐apoptotic Bcl‐2‐associated X protein (Bax) proteins and anti‐inflammatory mediators (IL‐10).