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To investigate the effects of Lycium barbarum polysaccharide (LBP) on pathological symptoms and behavioral deficits in a Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson’s disease (PD) mouse model. The therapeutic effects of LBP were monitored with an Open field test, a Rotarod test and a Morris water maze test. We also investigated the mechanisms with qRT-PCR and Western blotting analyses. After a relatively short-term LBP treatment, the total distance and walking time of PD mice significantly increased. The staying duration on the rod of PD mice increased in the Rotarod test. LBP can up-regulate levels of SOD2, CAT and GPX1 and inhibit the abnormal aggregation of α-synuclein induced by MPTP. LBP treatment can also up-regulate the phosphorylation of AKT and mTOR, and may play its protective role by activating the PTEN/AKT/mTOR signaling axis. These results suggest that LBP can effectively alleviate the degeneration in the nigrostriatal system induced by MPTP treatment. It may be a potential candidate for the treatment of Parkinson’s disease. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of flipped class in teaching of clinical anatomy for nursing students. Methods The participants were divided into the observation group (n = 63) and the control group (n = 60). Traditional teaching method was implemented in control group, while the clinical teaching based on flipped class was applied in observation group. The teaching outcomes were evaluated through students' performance in final exam and questionnaires survey about students' self-learning ability with the course. Results The scores of theoretic assessment and anatomical specimens identification in the observation group were higher than that in the control group (P < 0.05). The outcome of the survey revealed a high-level recognition of pre-class materials among students in the observation group. Students believed that flipped-class was potentially effective to improve the learning efficacy and self-competence. Conclusion The flipped-class method is effective to improve quality in teaching of clinical anatomy, and enhance the self-learning ability of nursing students. [ABSTRACT FROM AUTHOR]

Depression occurs in around 40 % of patients with Parkinson's disease (PD) and contributes to severe disability and a poor quality of life. The underlying mechanisms and pathophysiology of depression in PD (PDD) remain obscure, due to a lack of stable animal models of PDD. In this study, we established a PDD model by inducing exposure to chronic mild (CMS) and strong stress (CSS) using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in PD mice. We detected changes in motor and non-motor symptoms, brain structure, neurotransmitters, levels of 5-HT related genes and inflammation. CMS exposed PD (PDMS) mice exhibited obviously decreased levels of neuromuscular strength and enhanced levels of inflammation, compared with that of control mice. CSS exposed MPTP (PDSS) mice exhibited the highest level of motor impairment and depression states along with the highest levels of inflammation enhancement and a decrease in the expression levels of 5-hydroxytryptamine (5-HT) related genes in all groups. Our results suggested that CSS can successfully induce stable depression like symptoms in sub-chronic MPTP PD mice and appears to be a valuable tool for investigating PDD. Furthermore, it was found that 5-HT system dysfunction may contribute to depression like symptoms in PD. [ABSTRACT FROM AUTHOR]

Ample empirical evidence suggests that mitochondrial dysfunction and endoplasmic reticulum (ER) stress play a crucial role in the pathogenesis of Parkinson's disease (PD). Prohibitin (PHB), a mitochondrial inner-membrane protein involved in mitochondrial homeostasis and function, may be involved in the pathogenesis of PD. We investigated the functional role of PHB in mitochondrial biogenesis and ER stress in methyl-4-phenylpyridinium (MPP +)-induced in vivo and in vitro models of PD. The overexpression of PHB in SH-SY5Y cells block ed cell death and the apoptosis induced by MPP + incubation. PHB also block ed the activation of ER stress markers, including glucose-regulated protein 78, while increasing the expression of Xbox- binding protein 1 and caspase-12. Moreover, the intracerebroventricular administration of the PHB overexpression vector greatly block ed motor dysfunction and the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mediated neurodegeneration in the mouse model of PD. The production of reactive oxygen species, ER stress, and autophagic stress induced by MPTP were also significantly block ed in PD mice overexpressing PHB. Our results suggest that PHB blocks the dopaminergic-neuron depletion by preserving mitochondrial function and inhibiting ER stress. The genetic manipulation of PHB may feature potential as a treatment for PD., (Copyright © 2021 Elsevier B.V. All rights reserved.)