Title:Memory Enhancing and Neurogenesis Activity of Honey Bee Venom in the
Symptoms of Amnesia: Using Rats with Amnesia-like Alzheimer’s Disease
as a Model
Volume: 20
Issue: 3
关键词:
蜂毒，BDNF，DCX，阿尔茨海默病，神经退行性，脑源性神经营养因子。
摘要:
Background/Objective: Alzheimer's disease (AD) is mainly characterized by amnesia that
affects millions of people worldwide. This study aims to explore the effectiveness capacities of bee
venom (BV) for the enhancement of the memory process in a rat model with amnesia-like AD.
Methods: The study protocol contains two successive phases, nootropic and therapeutic, in which
two BV doses (D1; 0.25 and D2: 0.5 mg/kg i.p.) were used. In the nootropic phase, treatment groups
were compared statistically with a normal group. Meanwhile, in the therapeutic phase, BV was administered
to scopolamine (1mg/kg) to induce amnesia-like AD in a rat model in which therapeutic
groups were compared with a positive group (donepezil; 1mg/kg i.p.). Behavioral analysis was performed
after each phase by Working Memory (WM) and Long-Term Memory (LTM) assessments
using radial arm maze (RAM) and passive avoidance tests (PAT). Neurogenic factors; Brain-derived
neurotrophic factor (BDNF), and Doublecortin (DCX) were measured in plasma using ELISA and
Immunohistochemistry analysis of hippocampal tissues, respectively.
Results: During the nootropic phase, treatment groups demonstrated a significant (P < 0.05) reduction
in RAM latency times, spatial WM errors, and spatial reference errors compared with the normal
group. In addition, the PA test revealed a significant (P < 0.05) enhancement of LTM after 72 hours
in both treatment groups; D1 and D2. In the therapeutic phase, treatment groups reflected a significant
(P < 0.05) potent enhancement in the memory process compared with the positive group; less
spatial WM errors, spatial reference errors, and latency time during the RAM test, and more latency
time after 72 hours in the light room. Moreover, results presented a marked increase in the plasma
level of BDNF, as well as increased hippocampal DCX-positive data in the sub-granular zone within
the D1 and D2 groups compared with the negative group (P < 0.05) in a dose-dependent manner.
Conclusion: This study revealed that injecting BV enhances and increases the performance of both
WM and LTM. Conclusively, BV has a potential nootropic and therapeutic activity that enhances
hippocampal growth and plasticity, which in turn improves WM and LTM. Given that this research
was conducted using scopolamine-induced amnesia-like AD in rats, it suggests that BV has a potential
therapeutic activity for the enhancement of memory in AD patients in a dose-dependent manner
but further investigations are needed.
