In 42 male Wistar rats fed a high-fat diet for eight weeks to induce NAFLD, intraperitoneal crocin administered over four weeks significantly reduced hepatic lipid accumulation, normalized serum AST, ALT, and alkaline phosphatase levels, lowered malondialdehyde and nitrite concentrations, and restored antioxidant enzyme activity. Histopathological assessment confirmed measurable improvement in liver tissue morphology, including reduced steatosis and inflammatory infiltration.
Crocin is the primary carotenoid pigment in saffron and has attracted growing research interest for its antioxidant and anti-inflammatory properties. This finding adds to a body of preclinical literature suggesting that carotenoid-class compounds can interrupt the oxidative stress cascade central to NAFLD progression. The mechanism here likely involves crocin's free-radical scavenging capacity reducing lipid peroxidation — a key driver of hepatocyte injury and fibrosis.
However, the translational ceiling here is considerable. This is a rodent study using intraperitoneal injection — not oral supplementation — which bypasses first-pass metabolism and delivers doses that may be pharmacologically unrealistic for humans. With only seven animals per group, statistical power is limited, and no fibrosis endpoint was assessed. NAFLD in humans involves far more metabolic complexity than a simple high-fat diet model captures. Until randomized controlled trials confirm these effects in people — particularly on hard endpoints like liver fibrosis or cardiovascular risk — crocin remains a promising but unproven intervention. Incremental evidence, not yet practice-changing.