Abstract
Purpose: To explore the effects of octreotide (OCT) on oxidative stress, inflammation and apoptosis in hypoxia/reoxygenation (H/R)-induced cerebral infarction.Methods: The in vitro model of cerebral infarction was established by treating N2A cells with hypoxia for 4 h and reoxygenation for 24 h. The viability of N2A cells was determined by CCK-8 assay. The cells were divided into 3 groups: control group, H/R group, and H/R+OCT group. The cells in H/R+OCT group were pretreated with OCT (60 ng/mL) before H/R treatment. The oxidative stress of N2A cells were assessed by determining the levels of superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA). Inflammation of N2A cells was evaluated by evaluating the levels of TNF-α, IL-1β, IL-6, and IL-8, while the apoptosis of N2A cells was assessed by flow cytometry. Western blot analysis was used to determine the expression of Bcl-2, Bax, TLR4, MyD88, and NF-κB.Results: Octreotide treatment significantly reduced the level of oxidative stress. The inflammation of N2A cells caused by hypoxia/reoxygenation was inhibited by treatment with octreotide. Apoptosis of N2A cells was also inhibited by octreotide treatment. Hypoxia/reoxygenation activated TLR4/MyD88/NF-κB signaling pathway, while octreotide inhibits the activation of this pathway.Conclusion: The results reveal that octreotide inhibits hypoxia/reoxygenation-induced oxidative stress,as well as the inflammation, and apoptosis of N2A cells by inhibiting TLR4/MyD88/NF-κB signaling pathway. Thus, these findings may provide new insights into the treatment of cerebral infarction.
Highlights
Stroke is the second leading cause of death in the world
The total protein was extracted using cell lysis reagent (Thermo Fisher Scientific, Waltham, MA, USA) and the concentration was measured through the Bicinchoninic acid (BCA) kit according to the instructions of the supplier (Beyotime, Shanghai, China)
The hypoxia/reoxygenation (H/R) injury model was established, and the N2A cells were treated with different concentrations (20, 40, 60, 80, 100 ng/mL) of OCT
Summary
Stroke is the second leading cause of death in the world. It is the most serious and deadliest disease of the nervous system. After the ischemic brain tissue restores blood flow, reactive oxygen species (ROS) will be produced in large quantities, which in turn will aggravate nerve cell apoptosis and necrosis [2] This phenomenon is called cerebral ischemia/reperfusion injury [2]. The total protein was extracted using cell lysis reagent (Thermo Fisher Scientific, Waltham, MA, USA). While compared with the H/R group, the levels of ROS and MDA in the H/R + OCT group were significantly reduced (Figure 2 D and E) These results suggest that OCT can inhibit H/R-induced oxidative stress in N2A cells. The total protein was extracted using cell lysis reagent (Thermo Fisher Scientific, Waltham, MA, USA) and the concentration was measured through the Bicinchoninic acid (BCA) kit according to the instructions of the supplier (Beyotime, Shanghai, China).
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