Wasp Venom Ameliorates Scopolamine-Induced Learning and Memory Impairment in Mice.
Ji Hyeong ChaeJisun OhJi Sun LimYoon Ah JeongHyun Seok YunChan Ho JangHyo Jung KimJong-Sang KimPublished in: Toxins (2022)
This study investigated the effects of wasp venom (WV) from the yellow-legged hornet, Vespa velutina , on scopolamine (SCO)-induced memory deficits in mice, as well as the antioxidant activity in HT22 murine hippocampal neuronal cells in parallel comparison with bee venom (BV). The WV was collected from the venom sac, freeze-dried. Both venoms exhibited free radical scavenging capabilities in a concentration-dependent manner. In addition, the venom treatment enhanced cell viability at the concentrations of ≤40 µg/mL of WV and ≤4 µg/mL of BV in glutamate-treated HT22 cells, and increased the transcriptional activity of the antioxidant response element (ARE), a cis -acting enhancer which regulates the expression of nuclear factor erythroid 2-related factor 2 (Nrf2)-downstream antioxidant enzymes. Concurrently, WV at 20 µg/mL significantly increased the expression of a key antioxidant enzyme heme oxygenase 1 (HO-1) in HT22 cells despite no significant changes observed in the nuclear level of Nrf2. Furthermore, the intraperitoneal administration of WV to SCO-treated mice at doses ranged from 250 to 500 µg/kg body weight ameliorated memory impairment behavior, reduced histological injury in the hippocampal region, and reduced oxidative stress biomarkers in the brain and blood of SCO-treated mice. Our findings demonstrate that WV possess the potential to improve learning and memory deficit in vivo while further study is needed for the proper dose and safety measures and clinical effectiveness.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- high fat diet induced
- cell cycle arrest
- nuclear factor
- poor prognosis
- body weight
- ischemia reperfusion injury
- toll like receptor
- systematic review
- cell death
- gene expression
- high glucose
- anti inflammatory
- endoplasmic reticulum stress
- transcription factor
- working memory
- lipopolysaccharide induced
- wild type
- dna damage
- drug induced
- mouse model
- lps induced
- multiple sclerosis
- inflammatory response
- mass spectrometry
- long non coding rna
- functional connectivity
- endothelial cells
- high resolution
- cell proliferation
- brain injury
- resting state