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Nov 2021 DOI 10.14302/issn.2641-4538.jphi-21-3993
Adenike Adeyemo-Salami OluwatoyinCorresponding author
Nutritional and Industrial Biochemistry Unit, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan, Oyo State, Nigeria.
Chlorogenic acid (CA), abundantly found in green coffee beans, is a phenolic compound with antioxidant and anti-inflammatory properties amongst others. Exposure to rotenone, a natural pesticide, induces Parkinsonism (a type of neurodegeneration) through the induction of mitochondria dysfunction and oxidative stress. Phytochemicals with antioxidant properties may be promising in attenuating this condition. In this research, the ameliorative role of CA on rotenone-induced toxicity in Drosophila melanogaster was evaluated. Drosophila melanogaster (Harwich strain, 1- 3 days old) was used. 6 groups of five vials each with 50 flies/vial were exposed to CA (0; control (2% ethanol), 7.5, 15, 30, 45 and 60 mg/kg diet) for 28 days in the longevity analysis. A 28-day survival assay was carried out with rotenone (0, 250 and 500 μM). CA (30 mg/kg diet) was selected to evaluate its ameliorative potential on rotenone. For the study, the flies were divided into four groups of five vials each and exposed to CA and rotenone; Group A- control (2% ethanol), Group B- CA only, Group C- rotenone only and Group D- CA (30 mg/kg diet)+ rotenone (500 μM)for 7 days. Thereafter, the homogenate was evaluated for oxidative stress status, rate of emergence, negative geotaxis and acetyl cholinesterase activity. CA (30 mg/kg diet) extended the lifespan of flies by 21.4%. Also, CA ameliorated rotenone-induced perturbation in catalase, glutathione-S-transferase and acetyl cholinesterase activities, total thiol and glutathione levels, and behavioral deficit (p < 0.05). CA may have ameliorative effect against rotenone-induced toxicity and Parkinsonism.
Dec 2020 DOI 10.14302/issn.2577-2279.ijha-20-3634
Oloruntoba Adekeye AdeshinaCorresponding author
Department of Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria
The hippocampus is involved in learning and memory processes, an integral component of cognitive function. The aim of this study is to assess the efficacy of quercetin on manganese-induced neurotoxicity in the hippocampus of the adult mice. In this study, 40 adult mice of average weight of 18 –29g were randomly distributed into five groups of eight each. The brain was harvested and the region of the hippocampus was grossed for histological and immunohistochemical analysis. The results revealed a significant increased level of oxidative stress markers of manganese treated mice when compared with the normal control and quercetin treated animals (p<0.05). Immunohistochemical analysis also showed a decrease expression of Tumour necrosis factor alpha (TNFα) with quercetin treated animals when compared with manganese treated animals indicating its neuroprotective function. In addition, quercetin treated animals all had an improved working spatial memory in Y-maze test. The histological results also revealed a degeneration of pyramidal cells with a characteristic pyknotic activities at the granular layer of the hippocampus leading to neuronal integrity damage following chronic exposure to manganese but normal architectural design was however maintained with quercetin. Conclusively, exposure to manganese in excess may have adverse effect on extensive neuronal degeneration that could affect the learning, memory and possibly spatial navigation ability of miceand quercetin attenuates this induced neurotoxicity via inhibition of oxidative stress and reduction of TNF expression.
Feb 2017 DOI 10.14302/issn.2574-4372.jesr-16-1380
Wei HuafengCorresponding author
Department of Anesthesiology and Critical Care, Perelman School of Medicine,
General anesthetics (GAs) are widely used for various essential surgical or medical procedures. Recent studies implicate the GAs has dual effects of neuroprotection and neurotoxicity on neurogenesis with unclear mechanisms. This minireview summarizes recent studies on GAs mediated effects on neurogenesis and proposed mechanisms, with focus on autophagy regulation and intracellular calcium homeostasis.
Aug 2020 DOI 10.14302/issn.2641-7669.ject-20-3529
Wen XianjieCorresponding author
Department of Anesthesiology, the Second People`s Hospital of Foshan City, Foshan, Guangdong Province, China.
Background Local anesthetic neurotoxicity is a common complication in clinical anesthesia, which can cause permanent nerve damage in severe cases. The T-type calcium channel is an important channel for regulating the excitability of neurons. Normally, extracellular calcium ions enter the cell through the T-type calcium channel to change the excitability of neurons. When the intracellular calcium is overloaded, it can cause cell damage. Aims To investigated the roles of T-type calcium channel in the SH-SY5Y cells injury induced by the bupivacaine. Methods The SH-SY5Y cell culture model was used to observe the effect of T-type calcium channel blocker NNC55-0396 on the neurotoxicity of bupivacaine hydrochloride by MTT methold,flow cytometry, Western blotting and other methods. Results The results show that NNC55-0396 can block the T-type calcium channel of SH-SY5Y cells, improve the decrease of cell viability caused by bupivacaine hydrochloride, reduce the level of intracellular calcium ion, reduce the expression of Cleavedcaspase-3, and reduce cell apoptosis. Conclusion The above results indicate that the T-type calcium channel is involved in the SH-SY5Y cell damage caused by bupivacaine hydrochloride, and blocking the T-type calcium channel can reduce the neurotoxicity of bupivacaine hydrochloride.
Feb 2014 DOI 10.14302/issn.2328-0182.japst-13-206
C. García-Rodríguez J.Corresponding author
Life Sciences and Nanosecurity, Scientific Advisor’s Office.
The purpose of this study was to investigate the effect of cremophor RH-40 and polysorbate 80 with hydroxypropyl methylcellulose (HPMC) F4M on the development of formulations of intranasal erythropoietin with low sialic acid content (Neuro-EPO) as a neuroprotective agent. Parameters such as pH, osmolality, apparent viscosity, and protein concentration were controlled for minimizing the differences between formulations. All Neuro-EPO formulations showed similar behaviour in the physicochemistry quality control. However significant differences between formulations were observed in the permanent unilateral ischemia model. The formulations and the vehicles containing cremophor RH-40 showed higher neurotoxicity levels than those containing polysorbate 80 as a nonionic surfactant. Formulations containing HPMC F4M at 0.6% as a bioadhesive polymer showed higher levels of survival and better neurological status than those without the polymer. The formulations with polysorbate 80 and HPMC F4M showed a higher index of survival, smaller incidence of clinical signs of stroke, and similar behavior in the learning and the memory to the false injured animals used as control. These findings suggest that the intranasal pathway constitutes a safe and alternative route of access of the Neuro-EPO to the brain.