In vitro evaluation of the antifibrogenic effect of tamsulosin during its interaction with activated stellate cells

Introduction and Objective

Liver cirrhosis is a chronic disease that affects one-fifth of the world; in Mexico, it is the third cause of mortality. It is caused by the uncontrolled production of the extracellular matrix. Attempts have been made to develop treatments that can reverse this disease, attention has been paid to the stimuli responsible for the activation of hepatic stellate cells (HSC), and the presence of adrenoreceptors in these cells has also been demonstrated. This study aimed to demonstrate in the present work a possible treatment with a neuroimmune activity that decreases the fibrogenic capacity of HSC.

Material and Methods

Rat's HSC in a quiescent state and activated by primary culture were used. Cells in a quiescent state contain retinol and lose it by activation. The degree of activation was assessed by immunofluorescence for α-SMA and cytochemistry with Oil Red. Cell proliferation was assessed by the MTT reduction technique. Norepinephrine was used to activate adrenergic signaling and tamsulosin was used as an antagonist of this pathway.

Results

Initially, we standardized the primary culture of HSC, identified by the α-SMA marker at seven days of culture. Subsequently, it was demonstrated that Noradrenaline treatment activated stellate cells due to the progressive increase of α-SMA and its proliferation. Moreover, tamsulosin treatment was shown to decrease retinol loss by preventing its activation and reducing proliferation.

Conclusion

Tamsulosin has a direct effect on decreasing the activity of quiescent and activated HSCs.

Funding

The resources used in this study were from the hospital without any additional financing

Declaration of interest

The authors declare no potential conflicts of interest.