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Abstract The activation of hepatic stellate cells (HSCs) is a key event in the development of hepatic fibrosis caused by arsenic. However, it is unclear how arsenic induces the activation of HSCs. In the present study, we found that arsenic trioxide (As 2 O 3) induced liver tissue damage, stimulated autophagy and HSCs activation, and increased collagen accumulation in the liver of mice. Supplemented with taurine (Tau) attenuated the changes mentioned above caused by As 2 O 3. In human hepatic stellate cell line LX-2 cells, we found that As 2 O 3 -induced activation of HSCs was autophagy-dependent, and we found that peroxisome proliferator activated receptors alpha (PPARα) played an important role in arsenic-induced HSCs activation. In addition, inhibiting autophagy and PPARα alleviated the activation of HSCs and lipid droplet loss induced by As 2 O 3. Moreover, we found that Tau alleviated As 2 O 3 -induced elevation of autophagy and PPARα expression, and activation of the HSCs. Our results indicated that autophagy was regulated by PPARα and was involved in lipid droplet loss during the activation of HSCs. Tau alleviated As 2 O 3 -induced HSCs activation by inhibiting the PPARα/autophagy pathway. These findings give an innovative insight into the association of PPARα, autophagy, the activation of HSCs and hepatic fibrosis induced by As 2 O 3. Highlights • As 2 O 3 -induced the activation of hepatic stellate cells was autophagy-dependent. • PPARα played an important role in arsenic-induced HSCs activation. • Taurine decreased the level of autophagy, and inhibited the activity of hepatic stellate cells. [ABSTRACT FROM AUTHOR]