Hepatic stellate cells (HSC) are a nonparenchymal population of liver cells. In normal conditions, they store vitamin A, control the turnover of the extracellular matrix, and regulate the contractility of the sinusoids. Acute and chronic damage such as that brought about by alcohol activates the stellate cells and they are then responsible for the liver's inflammatory fibrotic response. Hence, alcohol consumption leads to hepatitis, steatosis, fibrosis and cirrhosis of liver by way of different mechanisms depending on effect upon the nonparenchymal cells of the liver.
The aim of our study was to assess the histological changes in the liver of rats after chronic alcohol consumption. In our work, we evaluated the intensity of liver fibrosis and the number of Kupffer cells and active hepatic stellate cells present within a test population. In the experiment, we used 10 Wistar rats of 250 gram weight. The animals were placed within one of two groups: A (experimental) and C (control). Group A received alcohol for 4 weeks, while group C received just water. The rats of both groups were decapitated 24 hours after the end of the experiment. The samples of liver were then evaluated after H&E, Masson’s trichrome staining and an immunohistochemical reaction to desmin (a marker of quiescent HSC) and α-smooth muscle actin (marker of active HSC) antibody. In our work, we observed intensive fibrosis in the portal spaces and perivenular areas in group A samples. Moreover, Kupffer cells and stellate cells with positive α-SMA expression were more numerous in group A than in the group C, and these correlate with the area of intensive fibrosis. The expression of desmin in the HSC was seen in both groups to a similar level.
Conclusion: Chronic alcohol consumption activates the transdifferentiation of hepatic stellate cells into the positive α-SMA myofibroblast-like cells which are responsible for fibrogenesis.