Abstract
Objective To explore the influences of protein kinase Cβ (PKCβ) inhibitor LY333531 on oxidative injury and apoptosis of SH-SY5Y cells induced by fluorosis. Methods The SH-SY5Y cell model of fluorosis was established, and the experiment was divided into three groups: control group [0.0 mmol/L sodium fluoride (NaF) and 0.0 μmol/L LY333531], the fluoride group (0.5 mmol/L NaF and 0.0 μmol/L LY333531), and the PKCβ inhibitor group (0.5 mmol/L NaF and 0.2 μmol/L LY333531), n= 3. Flow cytometry was used to detect the changes of reactive oxygen species (ROS) and apoptosis rate, fluorescent probe technique was used to detect mitochondrial membrane potential after each group for 48 h. Results Compared with the control group [(3.32 ± 0.29) × 103, 0.60 ± 0.09, (7.58 ± 1.20)%], the level of ROS [(5.99 ± 0.32) × 103] was increased, mitochondrial membrane potential (0.28 ± 0.06) was decreased, and the apoptosis rate [(18.00 ± 2.32)%] was increased in the fluoride group (all P < 0.05); compared with the fluoride group, the level of ROS [(5.12 ± 0.25) × 103] was decreased, mitochondrial membrane potential (0.42 ± 0.03) was increased, and the apoptosis rate [(11.79 ± 0.70)%] was decreased in the PKCβ inhibitor group (all P < 0.05). Conclusions Excess fluoride could cause oxidative damage and apoptosis in cells. PKCβ inhibitor LY333531 has a protective effect in oxidative damage and apoptosis by fluorosis. Key words: Fluoride; Reactive oxygen species; Apoptosis
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