IntroductionCell‐based therapy is considered as promising strategy to cure stroke. However, employing appropriate type of stem cell to fulfill many therapeutic needs of cerebral ischemia is still challenging. In this regard, the current study was designed to elucidate therapeutic potential of epidermal neural crest stem cells (EPI‐NCSCs) compared to bone marrow mesenchymal stem cells (BM‐MSCs) in rat model of ischemic stroke.MethodsIschemic stroke was induced by middle cerebral artery occlusion (MCAO) for 45 minutes. Immediately after reperfusion, EPI‐NCSCs or BM‐MSCs were transplanted via intra‐arterial or intravenous route. A test for neurological function was performed before ischemia and 1, 3, and 7 days after MCAO. Also, infarct volume ratio and relative expression of 15 selected target genes were evaluated 7 days after transplantation.ResultsEPI‐NCSCs transplantation (both intra‐arterial and intravenous) and BM‐MSCs transplantation (only intra‐arterial) tended to result in a better functional outcome, compared to the MCAO group; however, this difference was not statistically significant. The infarct volume ratio significantly decreased in NCSC‐intra‐arterial, NCSC‐intravenous and MSC‐intra‐arterial groups compared to the control. EPI‐NCSCs interventions led to higher expression levels of Bdnf, nestin, Sox10, doublecortin, β‐III tubulin, Gfap, and interleukin‐6, whereas neurotrophin‐3 and interleukin‐10 were decreased. On the other hand, BM‐MSCs therapy resulted in upregulation of Gdnf, β‐III tubulin, and Gfap and down‐regulation of neurotrophin‐3, interleukin‐1, and interleukin‐10.ConclusionThese findings highlight the therapeutic effects of EPI‐NCSCs transplantation, probably through simultaneous induction of neuronal and glial formation, as well as Bdnf over‐expression in a rat model of ischemic stroke.
Human physiological thermoregulation refers to four mechanisms: sweating, shivering, vasodilation and vasoconstriction. This active equilibrium, which maintains body temperature near 37°C, permits the
Feeding a moderately high-fat (MHF) diet in male Sprague-Dawley rats induces obesity, pressure natriuresis impairment and hypertension. This study investigated the role of the renal nerves in the impaired pressure natriuresis and hypertension caused by feeding a MHF diet. After collecting baseline data on day 0, 12 rats remained on a low-fat diet (LF group) while the others were switched onto a MHF diet and diverged into obesity-resistant (OR) or obesity-prone (OP). After 4 weeks, half of the OR and OP rats underwent bilateral renal denervation (BRD) to generate four groups: OR, OR/BRD, OP and OP/BRD (n = 12). During 10 weeks, body weight, obesity index, systolic pressure and renal excretory function were measured regularly. After 10 weeks, renal excretory responses to acute salt loading and renal autoregulation were evaluated. The OP and OP/BRD groups had greater increases of body weight and obesity index during the dietary period compared to the other groups, and by week 10 their body weight (425.1 ± 7.2 and 411.9 ± 5.1 g) became considerably larger than that of the LF group (358.5 ± 6.2 g). Renal sodium excretion was reduced by ∼20% at week 4 in the OP and OP/BRD groups, while only the OP group had lower sodium excretion at weeks 6-8 and higher systolic pressure over weeks 5-10 than the other groups and its week 10 systolic pressure reached 138.1 ± 6.7 versus 123.6 ± 2.7 mmHg of the LF group. The OP group showed delayed renal excretory responses to salt loading with rightward and downward shifts in renal autoregulatory curves. Therefore, the renal nerves exert a main mediatory role in the development of pressure natriuresis impairment and hypertension as obesity is established due to the long-term consumption of the MHF diet in male OP rats.
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