Abstract
Honeybee venom has recently been considered an anti-neurodegenerative agent, primarily due to its anti-inflammatory effects. The natural accumulation of amyloid-beta (Aβ) in the brain is reported to be the natural cause of aging neural ability downfall, and oxidative stress is the main route by which Aβ ignites its neural toxicity. Anti-neural oxidative stress is considered an effective approach for neurodegenerative therapy. To date, it is unclear how bee venom ameliorates neuronal cells in oxidative stress induced by Aβ. Here, we evaluated the neuroprotective effect of bee venom on Aβ-induced neural oxidative stress in both HT22 cells and an animal model. Our results indicate that bee venom protected HT22 cells against apoptosis induced by Aβ1–42. This protective effect was explained by the increased nuclear translocation of nuclear factor erythroid 2-like 2 (Nrf2), consequently upregulating the production of heme oxygenase-1 (HO-1), a critical cellular instinct antioxidant enzyme that neutralizes excessive oxidative stress. Furthermore, bee venom treatment activated the tropomyosin-related kinase receptor B (TrkB)/cAMP response element-binding (CREB)/brain-derived neurotrophic factor (BDNF), which is closely related to the promotion of cellular antioxidant defense and neuronal functions. A mouse model with cognitive deficits induced by Aβ1–42 intracerebroventricular (ICV) injections was also used. Bee venom enhanced animal cognitive ability and enhanced neural cell genesis in the hippocampal dentate gyrus region in a dose-dependent manner. Further analysis of animal brain tissue and serum confirmed that bee venom reduced oxidative stress, cholinergic system activity, and intercellular neurotrophic factor regulation, which were all adversely affected by Aβ1–42. Our study demonstrates that bee venom exerts antioxidant and neuroprotective actions against neural oxidative stress caused by Aβ1–42, thereby promoting its use as a therapeutic agent for neurodegenerative disorders.
Highlights
Maintaining the yin-yang balance has been a holistic approach in Korean medicine and traditional East Asian medicine to foster stable health, and a tilt in this stability would emerge as a disease condition in the human body [1]
Bee venom at 0.5–5 μg/mL exhibited a dose-dependent effect on HT22 cell availability at 12 to 24 h after Aβ1–42 challenge; this dosage was selected for later in vitro experiments (Figure 1A)
Our results show that bee venom demonstrated a potent neuroprotective effect in HT22 cells under Aβ1–42 stress induced via nuclear factor erythroid 2-like 2 (Nrf2)/heme oxygenase-1 (HO-1) upregulation and the tropomyosin-related kinase receptor B (TrkB)/cAMP response elementbinding (CREB)/brain-derived neurotrophic factor (BDNF) pathways
Summary
Maintaining the yin-yang balance has been a holistic approach in Korean medicine and traditional East Asian medicine to foster stable health, and a tilt in this stability would emerge as a disease condition in the human body [1]. In intrinsic neuro-aging, oxidative stress caused by naturally deposited Aβ in the human brain is considered the main cause of neurodegeneration [2,3]. Targeting the upregulation of endogenous antioxidant enzymes to neutralize excessive oxidative stress and invigorate neural cell redox balance has become a well-established approach to slow down the progression of neurodegenerative diseases [5–8]. This strategy interestingly reflects part of the East Asian medicine philosophy, a holistic therapy is not to focus on interacting directly with the disease itself but to reinforce the weakened half in the yin-yang balance to repel the illness by regaining energy harmony [9]. The present study on bee venom and its antioxidant properties in neurodegeneration provides an example of this focal point in Eastern and Western medical philosophy
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