BackgroundThe cognitive deficit has frequently been found in the elderly population. Several studies have shown that every single part of Moringa oleifera, including leaves, roots, and seeds, has abundant micronutrients, such as flavonoids, which improve the neurobehavioral capacity. However, herb parts that display optimal neuropharmacological properties remain unknown.ObjectiveWe investigate whether M. oleifera seed oil (MOO) or aqueous M. oleifera leaves extracts (MOEs) may ameliorate memory impairment in mice induced with scopolamine (Sco). Additionally, the phytochemical analyses of those two independent formulations were analyzed.MethodsIn this study, 2 ml/kg body weight (BW) of MOO and 500 mg/kg BW of MOE were orally administered to the mice for 28 days, followed by intraperitoneal injection of Sco (1 mg/kg) at the day 22–28 to induce cognitive impairment in those mice.ResultsThe Sco group showed memory retention impairment represented by the Y-maze and novel object recognition tests, significant enhancement of acetylcholine esterase (AChE) activity in hippocampus tissue (p < 0.0001), and increased the level of total antioxidant capacity (TAOC) in serum. Interestingly, the Sco-induced memory defect was improved and completely blunted the AChE exacerbation in Sco+MOO-treated mice (p < 0.0001), although the TAOC level was comparable among the groups. Mechanistically, both tropomyosin receptor kinase B (TrkB), as a brain-derived neurotrophic factor-receptor, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-κB) protein expressions were enhanced with the hippocampus isolated from the Sco group. Nonetheless, pretreatment with MOO only, but not with MOE, ameliorated the enhanced protein expression levels of TrkB and NF-κB (p < 0.05 and p = 0.09, respectively).ConclusionOur data reveal that MOO is preferable to MOE as a neuroprotective as evidenced by improving memory impairment. This effect, at least in part, through inhibiting the AChE and NF-κB activities and modulating the TrkB expression level.
Purpose Repeated stress events are well known to be associated with the onset of behavioral abnormalities including depression, anxiety and memory impairment. In spite of the traditional uses of Moringa oleifera (MO), no experimental evidence for its use against chronic stress exists. Here, we investigated whether seed oil from MO (MOO) could improve behavior abnormalities of chronic stress mice induced by water-immersion restraint stress (WIRS) and the underlying mechanism. Methods BALB/C male mice at 12 weeks of age were exposed to chronic WIRS for two weeks and divided in to four groups: normal group, WIRS group, WIRS+MOO1 group (treated with MOO at the dose of 1 mL/kg BW), and WIRS+MOO2 group (treated with MOO 2 mL/kg BW). The MOO treatment was given orally for 23 days. On day 24, we checked the behavior parameters, the plasma level of cortisol, acetylcholinesterase (AChE) activity in hippocampus, mRNA expression level of brain-derived neurotrophic factor ( BDNF ) and oxidative stress parameters in brain tissues. In addition, we also checked the histopathological features of the gastric mucosa wall. Results Administration of MOO ameliorated anxiety-like, depression-like and memory impairment phenotypes in the WIRS mouse model although the plasma cortisol concentrations were comparable among the groups. Of note, MOO both in two doses could suppress the AChE activity in hippocampus tissue and ameliorated the MDA level in prefrontal cortex tissue in mice exposed to WIRS. Although only WIRS+MOO2 group could increase the mRNA expression of BDNF , the histopathological gastric mucosa wall features were improved in all MOO groups. Conclusion Taken together, these finding suggested that MOO may have a neuroprotective effect in the mouse model of WIRS as evidenced by improving the abnormal behaviors through enhancing mRNA expression level of BDNF , inhibited AChE activity, and prevented the increase of MDA level in the brain.
Objective: To investigate the neuroprotective and antioxidant effects of leaves aqueous extract Moringa oleifera (MW) in chronic stress mouse models. Methods: Water immersion and stress restraint for 16 d to obtain a chronic stress model animal. Moringa extract flour dissolved in Aquades, dose 800 mg/kg for 23 d, for chronic Stress+MOW group. Fluoxetine in aquades at a dose of 18 mg/kg BW for 23 d for chronic stress group+Fluoxetine. Aquades were given to normal mice (group N), and mice under chronic stress conditions (chronic stress control group). Furthermore, measure behavioral abnormalities by testing depressive behavior and oxidative stress parameters such as anxiety, Brain-derived neurotrophic factors (BDNF). Results: Moringa oleifera water extract administration can improve behavioral disorders caused by stress by decreasing immobility time on the Force swim test, increasing time in the middle area, and increasing the number of returns to center areas on the Open field test. When chronically stressed mice were given fluoxetine and MOW, their MDA levels (p=0.008 and 0.041, respectively) and SOD activity (p=0.001 and 0.004) decreased significantly compared to the chronic stress control group. In contrast, Catalase activity increased significantly in chronically stressed mice given fluoxetine and MOW compared to the chronic stress control group (p=0.010 and 0.013). Administration of fluoxetine and MOW may increase the expression of mRNA BDNF compared to the chronic stress control group (p=0.000 and 0.013). Conclusion: The study found that MOW can improve behavioral abnormalities, namely anxiety and depression behavior caused by chronic stress exposure, through antioxidant pathways and oxidant systems, and also BDNF
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