Explore the Mechanism of β-Asarone on Improving Cognitive Dysfunction in Rats with Diabetic Encephalopathy

Abstract

Background: The number of people with diabetes is increasing, and many patients have significantly impaired cognitive function. For patients with diabetic encephalopathy (DE), simply lowering blood sugar does not improve learning and memory. Studies have shown that β-asarone can significantly improve cognitive impairment in patients with DE, but the specific mechanism of action is unclear. Objective: This experiment hopes to use a variety of experimental methods to clarify the protective effect and mechanism of β-asarone on brain neurons during the development of DE disease. Methods: A high-sugar and high-fat diet and streptozotocin injection-induced DE rat model was used. β-asarone was administered for four weeks. The experiment used the Morris water maze test, biochemical index detection, and many methods to evaluate the neuroprotective effect of β-asarone on DE rats from various aspects and understand its mechanism. Results: β-asarone reduced neuronal cell damage and significantly improved the learning and memory ability of DE rats. In addition, β-asarone can reduce the oxidative stress response and amyloid-β accumulation in the brain of DE model rats and increase the content of brain-derived neurotrophic factor (BDNF) in the brain tissue, thereby reducing neuronal cell apoptosis and playing a protective role. Conclusion: β-asarone can reduce the accumulation of oxidative stress and amyloid-β in the brain, increase the content of BDNF, reduce the apoptosis of neuronal cells, and exert neuronal protection, thereby improving the learning and memory ability of DE model rats.

β-Asarone Alleviates High-Glucose-Induced Oxidative Damage via Inhibition of ROS Generation and Inactivation of the NF-κB/NLRP3 Inflammasome Pathway in Human Retinal Pigment Epithelial Cells

“…In addition, β-asarone blocked the activation of NF-κB by HG and decreased the production and expression of IL-1β and IL-18, which are pro-inflammatory cytokines associated with NLRP3 inflammasome activation [15,16]. β-asarone inhibits HG-induced NLRP3 inflammasome activation in a myocardial I/R model [23]. These results imply that β-asarone protects ARPE-19 cells from HG-mediated oxidative stress, inflammation, and apoptosis via the regulation of NF-κB-related pathways.…”

“…Even with toxicological effects of β-asarone, it demonstrates therapeutic properties by targeting various pharmacological molecular targets such as apoptotic pathway modulator [20]. In particular, the antioxidant activity of β-asarone is related to the quenching of ROS generation in various experimental systems, including Alzheimer's disease and diabetic encephalopathy models [23,45,46]. Chang and Teng [47] reported that β-asarone inhibits the production of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), IL-1β, and IL-6, and induction of autophagy, while reducing apoptosis.…”

“…In addition, β-asarone directly scavenges hydrogen peroxide and hydroxyl radicals and exerts protective effects against DNA oxidation [22]. Recently, Cai et al [23] reported that a decrease in amyloid-β-induced neuronal apoptosis and improvement in learning and memory by β-asarone were closely related to the reduction in oxidative stress. Xiao et al [24] revealed that β-asarone mitigates myocardial ischemia/reperfusion (I/R) injury via the inhibition of NLRP3 inflammasome-mediated lytic cell death.…”