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ROS-mediated actin-cytoskeleton disarrangements were fully prevented by both PKC-pan-specific and cPKC-specific inhibitors.98 What is more relevant from the therapeutic point of view, both cytoskeleton disruption and canalicular dysfunction are reversed within 1 h by these inhibitors.98 The retrieval of the bile salt transporter, Bsep, from the canalicular membrane was also fully prevented by PKC antagonists.109 The same holds true for the impairment of the tight-junctional-retentive properties, another possible consequence of the actin disassembly induced by exposure to pro-oxidant agents.98 The exact mechanisms that explain the harmful effect of PKC on actin integrity and, by extension, to the hepatocanalicular function as a whole are unclear
