Key result
Glabridin supplementation at 40 mg/kg daily markedly reduced collagen fiber deposition in the periportal space (38.36 vs 70.71 µm) and significantly decreased collagen type I and fibronectin expression in diabetic rats.
Why the study?
Hyperglycemia in diabetes induces organ destruction and excessive collagen deposition in chronic liver disease, prompting investigation into whether glabridin could decrease hepatocyte destruction and collagen deposition in diabetic liver tissue.
Does glabridin reduce liver collagen deposition and hepatocyte destruction in streptozotocin-induced diabetic rats?
Does glabridin reduce liver collagen deposition and hepatocyte destruction in streptozotocin-induced diabetic rats?
Answers are grounded in this paper and cite their sources.
Glabridin supplementation attenuates liver fibrosis and hepatocyte damage in a rat model of streptozotocin-induced diabetes.
Abnormalities in insulin hormone levels leads to a hyperglycemic condition of diabetic mellitus. Hyperglycemia seriously induces organ and system destructions. The excessive accumulation of collagen fiber deposits occurs in inflammatory and reorganization processes of chronic liver diseases in type I insulin-dependent diabetes. Regarding the research objective, glabridin (GLB), an active compound of licorice, was used as a daily supplement (40 mg/kg) in order to decrease hepatocyte destruction and collagen deposition in liver tissue of diabetic animals induced by streptozotocin. A total of 40 were randomly allocated to five groups (each, n=10), control, control treated with GLB (GLB), diabetic rats (DM) injected with single dose of streptozotocin (60 mg/kg) to induce a diabetic condition, diabetic rats receiving GLB (DM+GLB; 40 mg/kg) and diabetic rats treated with glibenclamide (DM+GL; 4 mg/kg). Characteristic histopathological changes in liver cells and tissues of rats were determined by Masson's trichrome staining and transmission electron microscopy (TEM). Western blotting was used to detect the expression of the key markers, collagen type I and fibronectin proteins. The histological investigation of liver tissue of the DM group revealed that the collagen fiber deposition was increased in the periportal, pericentral and perisinusoidal spaces compared with controls. Hepatocytes appeared as small and fragmented cells in TEM examination. Collagenization of the perisinusoidal space was recently demonstrated to represent a new aspect of the microvascular abnormalities and liver fibrosis. Healthy hepatocytes with round nucleus were observed following supplementation of glabridin. In addition, collagen fiber deposition was reduced in the area adjacent to the perisinusoidal space. The expression of collagen type I and fibronectin decreased strongly following glabridin supplementation in DM+GLB rats compared with DM rats, indicating that the hepatic tissue reorganization regained its normal morphology. These findings suggest that it may be beneficial to examine the role of glabridin as a therapeutic agent in diabetes treatment in future research.
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Komolkriengkrai et al. (2019) studied Streptozotocin-induced diabetes mellitus (n=40). Glabridin vs. Untreated diabetic rats (DM) was evaluated on Thickness of collagen deposition in periportal space (PT). Glabridin supplementation at 40 mg/kg daily markedly reduced collagen fiber deposition in the periportal space (38.36 vs 70.71 µm) and significantly decreased collagen type I and fibronectin expression in diabetic rats.
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