DJ-1/PARK7, the Parkinson's disease-related protein, plays an important role in mitochondrial function. However, the mechanisms by which DJ-1 affects mitochondrial function are not fully understood. Akt is a promoter of neuron survival and is partly involved in the neurodegenerative process. This research aimed at investigating a possible relationship between DJ-1 and Akt signalling in regulating mitochondrial function in the dopaminergic neuron-like cells SH-SY5Y and PC-12. Overexpression of DJ-1 was firstly validated at both the transcriptional and translational levels after transit transfection with plasmid pcDNA3-Flag-DJ-1. Confocal fluorescence microscopy demonstrated that overexpression of DJ-1 increased the mitochondrial mass, but did not disrupt the mitochondrial morphology. In addition, mitochondrial complex I activity was raised in DJ-1-overexpressing cells, and this rise occurred with an increase in cellular adenosine 5'-triphosphate content. Moreover, immunoblotting demonstrated that the levels of phosphoinositide 3-kinase and the total Akt were not altered in DJ-1-overexpressing cells, and nor was the Akt phosphorylation on serine 473 changed. By contrast, Akt phosphorylation on threonine 308 was significantly augmented by overexpression of DJ-1, and the expression of glycogen synthase kinase-3beta, a downstream effector of Akt, was suppressed. In summary, these results suggest that overexpression of DJ-1 improves the mitochondrial function, at least in part, through a mechanism involving Akt phosphorylation on threonine 308.

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ObjectivesMental health problems among university students are a cause of widespread concern. Mindfulness-based interventions (MBIs) delivered online have considerable potential to help university students manage mental health challenges. However, there is no consensus regarding the efficacy of online MBIs. This meta-analysis aims to determine whether MBIs are feasible and effective for improving university students’ mental health.MethodsRandomised controlled trials (RCTs) in Web of Science, PubMed, Cochrane Library, Embase and the US National Library of Medicine (Clinical Trial Registry) published through August 31, 2022, were searched. Two reviewers selected the trials, conducted a critical appraisal, and extracted the data. Nine RCTs met our inclusion criteria.ResultsThis analysis showed that online MBIs were effective in improving depression (standardised mean difference [SMD] = −0.27; 95% confidence interval [CI], −0.48 to −0.07; P = 0.008), anxiety (SMD = −0.47; 95% CI, −080 to −0.14; P = 0.006), stress (SMD = −0.58; 95% CI, −0.79 to −0.37; P < 0.00001), and mindfulness (SMD = 0.71; 95% CI, 0.17 to 1.25; p = 0.009) in university students. No significant effect was found on wellbeing (SMD = 0.30; 95% CI, −0.00 to 0.60; P = 0.05).ConclusionThe findings indicated that online MBIs could effectively improve the mental health of university students. Nevertheless, additional rigorously designed RCTs are required.Systematic review registrationhttps://inplasy.com/inplasy-2022-9-0099/, identifier INPLASY202290099.

Da-Bu-Yin-Wan (DBYW) and Qian-Zheng-San (QZS), two classic traditional Chinese medicinal formulas, were clinically employed to treat Parkinson's disease (PD). Our previous studies demonstrated neuroprotective effects of them on mitochondrial function in PD mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The purpose of this research was to investigate their possible mechanisms in the light of mitochondrial ATP-sensitive potassium (mitoKATP) channels. The neuroprotective effect of DBYW and QZS on dopamine (DA) neurons in substantia nigra (SN) in the MPTP-induced PD mice was investigated by behavioral test (pole test) and immunohistochemistry. Adenosine triphosphate (ATP) level in the midbrain tissue was detected by firefly luciferase method. MitoKATP channel subunits SUR1 and Kir6.2 mRNA and protein expressions were tested by real-time PCR (RT-PCR) and Western blot. It was observed that DBYW and/or QZS served to ameliorate MPTP-induced behavioral impairment and prevent the loss of substantia nigra dopamine neurons, as well as increase ATP level in the midbrain tissue and downregulate SUR1 expression at mRNA and protein levels with no marked influence on Kir6.2. We concluded that DBYW and QZS exhibit neuroprotective effects probably through the regulation of ATP level and mitoKATP channel subunit expressions.

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