Neuroprotective effect of combined therapy with hyperbaric oxygen and madopar on 6-hydroxydopamine-induced Parkinson’s disease in rats

Pan, Xiaorong; Chen, Chunxia; Huang, Jianping; Wei, Haiming; Qing, Fan

doi:10.1016/j.neulet.2015.06.030

Cited by 31 publications

(21 citation statements)

References 32 publications

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“…In our study, D * -values were lower in the Madopar group than that of the PD group, but were not significantly different between the Madopar group and the sham or control groups. It can be inferred that Madopar treatment partially preserved dopaminergic neurons, which was consistent with previous work (Pan et al, 2015) as well as other findings in our study. Yet, our observation of increased k'-values in the PD group compared to other groups was inconsistent with previous research reporting reduced k'-values in the SN of PD model rats; it was proposed that glial cell hyperplasia in the SN area and waste accumulation (e.g., reduced α-synclearance) in the SN was responsible for decreased k'-values (Ren et al, 2016).…”

Section: Discussionsupporting

confidence: 94%

Altered Tracer Distribution and Clearance in the Extracellular Space of the Substantia Nigra in a Rodent Model of Parkinson's Disease

et al. 2017

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The relationship between extracellular space (ECS) diffusion parameters and brain drug clearance is not well-studied, especially in the context of Parkinson's disease (PD). Therefore, we used a rodent model of PD to explore the distribution and clearance of a magnetic resonance tracer. Forty male Sprague Dawley rats were randomized into four different groups: a PD group, a Madopar group (PD + Madopar treatment), a sham group, and a control group. All rats received an injection of the extracellular tracer gadolinium-diethylene triaminepentacetic acid (Gd-DTPA) directly into the substantia nigra (SN). ECS diffusion parameters including the effective diffusion coefficient (D*), clearance coefficient (k'), ratio of the maximum distribution volume of the tracer (Vd-max%), and half-life (t1/2) were measured. We found that all parameters were significantly increased in the PD group compared to the other three groups (D*: F = 5.774, p = 0.0025; k': F = 20.00, P < 0.0001; Vd-max%: F = 12.81, P < 0.0001; and t1/2: F = 23.35, P < 0.0001). In conclusion, the PD group exhibited a wider distribution and lower clearance of the tracer compared to the other groups. Moreover, k' was more sensitive than D* for monitoring morphological and functional changes in the ECS in a rodent model of PD.

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Section: Discussionsupporting

confidence: 94%

Altered Tracer Distribution and Clearance in the Extracellular Space of the Substantia Nigra in a Rodent Model of Parkinson's Disease

et al. 2017

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“…This novel model promotes lifelong Parkinsonian symptoms without the characteristic motor deficits observed in PD, providing a truly unique system to study Parkinson's disease progression. Other studies aimed at reducing the oxidative stress promoted by 6-OHDA induction include the administration of antioxidants that also have anti-inflammatory properties such as echinacoside [ 526 ], PEG conjugated recombinant human FGF-2 [ 527 ], madopar (a combination of the dopamine precursor, levodopa, and benserazide, a decarboxylase inhibitor) [ 528 ], guanosine, an MPP + antagonist [ 529 ], and carnosine [ 530 ]. A safe, effective, combinatorial therapy of GAD and AAV2 vector which codes for the dopamine synthetic enzyme, aromatic-l-amino decarboxylase (AADC), has yielded encouraging results in a small number of PD patients by improving motor performance [ 531 , 532 ].…”

Section: An Overview Of Some Neurodegenerative Diseasesmentioning

confidence: 99%

Role of ROS and RNS Sources in Physiological and Pathological Conditions

Meo

Reed

Venditti

et al. 2016

Oxidative Medicine and Cellular Longevity

1,178

667

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There is significant evidence that, in living systems, free radicals and other reactive oxygen and nitrogen species play a double role, because they can cause oxidative damage and tissue dysfunction and serve as molecular signals activating stress responses that are beneficial to the organism. Mitochondria have been thought to both play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction through several mechanisms, including stimulation of opening of permeability transition pores. Until recently, the functional significance of ROS sources different from mitochondria has received lesser attention. However, the most recent data, besides confirming the mitochondrial role in tissue oxidative stress and protection, show interplay between mitochondria and other ROS cellular sources, so that activation of one can lead to activation of other sources. Thus, it is currently accepted that in various conditions all cellular sources of ROS provide significant contribution to processes that oxidatively damage tissues and assure their survival, through mechanisms such as autophagy and apoptosis.

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“…Immunohistochemical procedures were conducted according to the method of a previous study [16]. Briefly, the waxed and dehydrated specimens were incubated with primary antibody overnight at 4°C.…”

Section: Immunohistochemistry Of Bax and Bcl-2 Expressionmentioning

confidence: 99%

Cardioprotective Effects of Combined Therapy with Hyperbaric Oxygen and Diltiazem Pretreatment on Myocardial Ischemia-Reperfusion Injury in Rats

Chen

Nong³

et al. 2016

Cell Physiol Biochem

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Background/Aims: In this study, we examined whether the combination of hyperbaric oxygen (HBO) and diltiazem therapy provided a cardioprotective effect on myocardial ischemia-reperfusion injury (MIRI) rat model. Methods: Sixty healthy Sprague-Dawley rats were randomly divided into sham, IR, diltiazem (5 mg/kg), HBO (0.25 MPa, 60 min) and combination therapy (HBO plus diltiazem) groups. MIRI model was established by ligating the left anterior descending for 30 min, followed by 60 min of reperfusion. Results: The results show that HBO and diltiazem preconditioning significantly improves cardiac function and myocardial infarction area, increases nitric oxide, endothelial nitric oxide synthase and ATPase (Na⁺-K⁺-ATPase and Ca²⁺-Mg²⁺-ATPase) activity and decreases levels of oxygen stress, myocardial enzymes and endothelin-1. Notably, HBO and diltiazem preconditioning significantly increased Bcl-2 protein expression and decreased Bax protein and caspase-3 mRNA expression. Conclusions: These data indicate that combination therapy protected against heart MIRI by reducing oxygen stress damage, correcting energy metabolism, improving endothelial function and inhibiting cell apoptosis.

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Neuroprotective effect of combined therapy with hyperbaric oxygen and madopar on 6-hydroxydopamine-induced Parkinson’s disease in rats

Cited by 31 publications

References 32 publications

Altered Tracer Distribution and Clearance in the Extracellular Space of the Substantia Nigra in a Rodent Model of Parkinson's Disease

Altered Tracer Distribution and Clearance in the Extracellular Space of the Substantia Nigra in a Rodent Model of Parkinson's Disease

Role of ROS and RNS Sources in Physiological and Pathological Conditions

Cardioprotective Effects of Combined Therapy with Hyperbaric Oxygen and Diltiazem Pretreatment on Myocardial Ischemia-Reperfusion Injury in Rats

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