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  • br Materials and methods br Results br Discussion br

    2021-09-03


    Materials and methods
    Results
    Discussion
    Acknowledgments
    Introduction As we move into an aging society, there has been a growing interest in neurological disorders [1]. Neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD) cause cognitive malfunction and behavioral impedance, often devastating the lives of patients [2], [3]. In the case of dementia, brain lesions in the cerebral cortex accelerate memory deficits and impairment of abstract thinking and can lead to spatial and linguistic disorders. Various medicinal plants have traditionally been applied to treat neurodegenerative diseases [4], [5]. Natural compounds from plants tend to have weaker potency than synthetic compounds but can provide long-term benefits without severe side effects [6]. Six different types of lamiaceae have been previously used, including Origanum vulgare L. (oregano) 12.40 mg/g, Hyssopus officinalis L. (hyssop) 7.84 mg/g, Ocimum basilicum L. (basil) 3.59 mg/g, Rosmarinus officinalis L. (rosemary) 1.33 mg/g, Melissaofficinalis L. (lemon balm) 2.85 mg/g, and Salvia officinalis L. (sage) 2.12 mg/g (rosmarinic 8-Bromo-cGMP, sodium salt australia content in ethanol extraction) [7]. We applied 50–100 mg/kg in ip treatment and 25 μM in cell treatment [8]. Among these medicinal plants were herbs such as peppermint and spearmint. Also included was rosemary, from the subfamily Nepetoideae of the Lamiaceae, the main ingredient of which is rosmarinic acid (RA) [9]. RA is known to have antioxidative and anti-inflammatory effects. In addition to this, the neuroprotective effects of RA have been confirmed in a temporal lobe epilepsy rat model [10]. Furthermore, anti-depressive effects were also previously reported from behavior tests conducted in mice treated with RA [11]. In PC-12 cells, RA increased the expression of the tyrosine hydroxylase (TH) and pyruvate carboxylase (PC) and decreased that of MKP-1. Moreover, changes in neurotransmitters like TH and PC have also been observed in PC-12 cells treated with rosemary extract [8]. These results show that RA treatment increased release of those neurotransmitters and mRNA level of BDNF in the limbic area. It implies potential contribution of RA to LTP formation, since BDNF increases LTP via a signaling pathway by binding to TrkB or BDNF receptors [12], [13]. LTP consists of strong depolarization caused by glutamate release from presynaptic neurons and binding of postsynaptic glutamate receptors [14]. In 1973, Bliss and Lomo found that brief trains of high-frequency stimulation applied to excitatory afferents in the hippocampus caused an increase in synaptic transmission [15]. It is generally accepted that the induction of LTP at a synapse requires activation of postsynaptic NMDA receptors through sufficient glutamate release during depolarization. This results in the relief of the voltage-dependent blockage of NMDA receptor by extracellular Mg2+, which in turn permits the entry of Ca2+ into the postsynaptic dendrite spine [16]. Within the dendritic spine, Ca2+ then binds to calmodulin (CaM) to activate CaMKII, which undergoes autophosphorylation, thus maintaining its activity even after Ca2+ returns to basal level. CaMKII phosphorylates AMPA receptors (AMPARs) already present in the synaptic plasma membrane, thus increasing membrane conductance by opening channels. CaMKII is also postulated to influence subsynaptic localization of AMPA receptors in order to recruit more AMPA receptors to the synaptic plasma membrane [17]. In this study, we evaluated the effects of RA on LTP and its neuroprotective activity in a scopolamine-induced memory impairment model.
    Materials and methods
    Results
    Discussion Numerous studies have shown evidence of the effects of rosmarinic acid (RA) on BDNF expression and neurotransmitter release [8], [24]. It is also known that RA can increase long-term plasticity (LTP) and has neuroprotective activities in a scopolamine-induced memory impairment model. In this study, RA indeed increased the expression of BDNF in hippocampal tissue (Fig. 3C and D). These results were similar to those of the previous reports, especially in the aspects of electrophysiology. GluR-2 was also increased by RA treatment, which has an important implication in synaptic plasticity since GluR-2 controls AMPA receptor assembly and trafficking [25].