Diabetes mellitus (DM) is a chronic metabolic disorder associated with hepatic dysfunction caused by persistent oxidative stress and hyperglycemia. The establishment of safe plant-based therapies to manage diabetes-related hepatic injury has been an important research area. This experimental study determined the hepatoprotective effect of Cichorium intybus (Kasni) seed extract on alloxan-induced diabetes in mice via histopathological evaluation. Thirty male albino mice were selected and randomly divided into three groups (n = 10 each): the nondiabetic control group, the diabetic untreated group, and the diabetic Kasni-treated group. Type 2 diabetes was induced by the intraperitoneal administration of alloxan monohydrate (150 mg/kg). Aqueous extracts of Kasni seeds (400 mg/kg) were orally administered once a day for 28 days to the mice in the treatment group, and gross liver morphology and histological features were studied for changes via hematoxylin and eosin (H&E) staining. The results of the present study revealed that untreated diabetic mice presented elevated blood glucose levels, enlarged pale livers, and histological features indicating hepatic injury, including hepatocellular vacuolation, sinusoidal congestion, and early pericentral fibrosis. Diabetic mice treated with Kasni presented near-normal hepatic histological features; furthermore, the structure of the central vein was restored, orderly hepatocyte plates formed, and no inflammation, steatosis or fibrosis was observed. The gross morphological features revealed that the liver color and texture were similar to those of the control group. The study concluded that Cichorium intybus has a hepatoprotective effect against diabetes-related liver damage because of the antioxidant and anti-inflammatory properties of the active ingredients in the plant.

Excess fructose intake is a main contributor to metabolic syndrome, which causes dyslipidemia, nonalcoholic fatty liver disease (NAFLD) and insulin resistance. The present study examined the protective effects of quercetin, quinoa seed extract (QSE), and kaempferol against high-fructose diet (HFrD)-induced pancreatic and hepatic alterations in Wistar albino rats. Thirty rats were divided into six groups (n = 5, each group consisted of 5 rats): the control group, HFrD + metformin group, HFrD + kaempferol group, HFrD + quercetin group, and HFrD + QSE group. Treatments were administered orally for 21 days following induction with 61% fructose. Biochemical function tests were performed for hemoglobin (Hb) and alanine aminotransferase (ALT) levels, and histopathological analyses of hepatic and pancreatic architecture were performed. The results showed that HFrD intake significantly increased ALT levels and body weight, accompanied by hepatocellular degeneration and inflammatory changes in pancreatic β-cells. Kaempferol, quercetin, and QSE administration significantly increased the Hb concentration, decreased ALT activity, and reduced vacuolar degeneration and hepatic necrosis. Kaempferol and quercetin resulted in nearly normal hepatocyte morphology among the test compounds, while QSE resulted in the greatest decrease in net weight gain. In the treated groups, pancreatic sections revealed the integrity of the islets of Langerhans and decreased inflammation of the islets. This study demonstrated that flavonoids from plants and the QSE have hepatoprotective and pancreatic protective effects through antioxidant and anti-inflammatory mechanisms; hence, these compounds are potentially useful as therapeutic agents in the management of fructose-induced metabolic dysfunctions.