Experimental research Effects of intravenous human umbilical cord blood CD34+ stem cell therapy versus levodopa

Abstract

IntroductionParkinsonism is a neurodegenerative disease with impaired motor function. The current research was directed to investigate the effect of CD34+ stem cells versus levodopa in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism.Material and methodsMice were divided into 4 groups; saline-injected, MPTP: received four MPTP injections (20 mg/kg, i.p.) at 2 h intervals, MPTP groups treated with levodopa/carbidopa (100/10 mg/kg/twice/day for 28 days) or single intravenous injection of 106 CD34+ stem cells/mouse at day 7 and allowed to survive until the end of week 5.ResultsLevodopa and stem cells improved MPTP-induced motor deficits; they abolished the difference in stride length, decreased percentage of foot slip errors and increased ambulation, activity factor and mobility duration in parkinsonian mice (p < 0.05). Further, they significantly (p < 0.05) increased striatal dopamine (85.3 ±4.3 and 110.6 ±5.3) and ATP levels (10.6 ±1.1 and 15.5 ±1.14) compared to MPTP (60.1 ±3.9 pmol/g and 3.6 ±0.09 mmol/g, respectively) (p < 0.05). Moreover, mitochondrial DNA from mice treated with levodopa or stem cells was in intact form; average concentration was (52.8 ±3.01 and 107.8 ±8.6) and no appreciable fragmentation of nuclear DNA was found compared to MPTP group. Regarding tyrosine hydroxylase (TH) immunostaining, stem cell group showed a marked increase of percentage of TH-immunopositive neurons (63.55 ±5.2) compared to both MPTP (37.6 ±3.1) and levodopa groups (41.6 ±3.5).ConclusionsCD34+ cells ameliorated motor, biochemical and histological deficits in MPTP-parkinsonian mice, these effects were superior to those produced by levodopa that would be promising for the treatment of PD.

Plasma derived from human umbilical cord blood: Potential cell‐additive or cell‐substitute therapeutic for neurodegenerative diseases

“…| 6163 IL-8 and VEGF might be a beneficial treatment for repair of the damaged blood-brain barrier and/or blood-spinal cord barrier in patients with ALS, [41][42][43][44] AD, 45 Parkinson's disease 46 and multiple sclerosis. 47 Finally, our in vitro studies showed significantly increased viabil- In this context, numerous studies have shown neuroprotective effects of MNC hUCB administered into animal models of ALS, [48][49][50][51] AD, [52][53][54] Parkinson's disease, 55 ischaemic stroke 56,57 and traumatic brain injury. 58 been observed from intravenous administration of CBP into rats modelling acute ischaemic stroke 5 or into an animal model of ageing.…”

Systemic Human CD34 + Cells Populate the Brain and Activate Host Mechanisms to Counteract Nigrostriatal Degeneration

“…Among the mononuclear cell types, particularly CD34 + cells, which are primitive hematopoietic and endothelial cell progenitors, have shown a strong ability to stimulate endogenous cell survival promoting mechanisms such as neurogenesis, angiogenesis and inflammatory modulation to induce neuroprotection [14][15][16]24,29,30]. In fact in PD models, reports indicate that intravenously administered CD34 + hCBCs can support the survival of SN TH + DA neurons and induce behavioral improvements in the animals [31][32][33]. However, the mechanisms underlying the neuroprotective and functional effects of the systemic hCBCs are not well understood.…”

Hyperbaric oxygen effects on the alveoli-capillary unit in a murine model of pulmonary arterial hypertension

“…The CD34+ vascular pluripotent cells synthesise several vascular cell markers, as well as proteins related to vasculogenesis and smooth muscle differentiation. CD34-cells consist of a mixed population that over-synthesises factors that can promote angiogenesis [32][33][34].…”