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Sharma, Hari Shanker
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Publications (10 of 210) Show all publications
Wiklund, L., Patnaik, R., Sharma, A., Miclescu, A. & Sharma, H. S. (2018). Cerebral Tissue Oxidative Ischemia-Reperfusion Injury in Connection with Experimental Cardiac Arrest and Cardiopulmonary Resuscitation: Effect of Mild Hypothermia and Methylene Blue. Molecular Neurobiology, 55(1), 115-121
Open this publication in new window or tab >>Cerebral Tissue Oxidative Ischemia-Reperfusion Injury in Connection with Experimental Cardiac Arrest and Cardiopulmonary Resuscitation: Effect of Mild Hypothermia and Methylene Blue
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 115-121Article in journal (Refereed) Epub ahead of print
Abstract [en]

The present investigation is an expansion of previous studies which all share a basic experimental protocol of a porcine-induced cardiac arrest (CA) of 12 min followed by 8 min of cardiopulmonary resuscitation (CPR), different experimental treatments (immediate as well as postponed induced mild hypothermia and administration of much or less cool intravenous fluids), and a follow-up period of 3 h after which the animals were sacrificed. Another group of animals was studied according to the same protocol after 12-min CA and Bstandard CPR.^ After death (within 1 min), the brains were harvested and frozen in liquid nitrogen awaiting analysis. Control brains of animals were collected in the same way after short periods of untreated CA (0 min, 5 min, and 15–30 min). Previous studies concerning chiefly neuropathological changes were now expanded with analyses of different tissue indicators (glutathione, luminol, leucigenin, malonialdehyde, and myeloperoxidase) of cerebral oxidative injury. The results indicate that a great part of oxidative injury occurs within the first 5 min after CA. Immediate cooling by administration of much intravenous fluid results in less cerebral oxidative injury compared to less intravenous fluid administration. A 30-min postponement of induction of hypothermia results in a cerebral oxidative injury comparable to that of Bstandard CPR^ or the oxidative injury found after 5 min of untreated CA. Intravenous administration of methylene blue (MB) during and immediately after CPR in combination with postponed cooling resulted in no statistical difference in any of the indicators of oxidative injury, except myeloperoxidase, and glutathione, when this treatment was compared with the negative controls, i.e., animals subjected to anesthesia alone.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
Cardiac arrest, Oxidative injury, Ischemia reperfusion, Methylene blue
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:uu:diva-337384 (URN)10.1007/s12035-017-0723-z (DOI)000424702600012 ()28895060 (PubMedID)
Available from: 2017-12-24 Created: 2017-12-24 Last updated: 2018-04-04Bibliographically approved
Huang, H., Young, W., Chen, L., Feng, S., Al Zoubi, Z. M., Sharma, H. S., . . . Li, T. (2018). Clinical Cell Therapy Guidelines for Neurorestoration (IANR/CANR 2017). Cell Transplantation, 27(2), 310-324
Open this publication in new window or tab >>Clinical Cell Therapy Guidelines for Neurorestoration (IANR/CANR 2017)
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2018 (English)In: Cell Transplantation, ISSN 0963-6897, E-ISSN 1555-3892, Vol. 27, no 2, p. 310-324Article, review/survey (Refereed) Published
Abstract [en]

Cell therapy has been shown to be a key clinical therapeutic option for central nervous system diseases or damage. Standardization of clinical cell therapy procedures is an important task for professional associations devoted to cell therapy. The Chinese Branch of the International Association of Neurorestoratology (IANR) completed the first set of guidelines governing the clinical application of neurorestoration in 2011. The IANR and the Chinese Association of Neurorestoratology (CANR) collaborated to propose the current version "Clinical Cell Therapy Guidelines for Neurorestoration (IANR/CANR 2017)". The IANR council board members and CANR committee members approved this proposal on September 1, 2016, and recommend it to clinical practitioners of cellular therapy. These guidelines include items of cell type nomenclature, cell quality control, minimal suggested cell doses, patient-informed consent, indications for undergoing cell therapy, contraindications for undergoing cell therapy, documentation of procedure and therapy, safety evaluation, efficacy evaluation, policy of repeated treatments, do not charge patients for unproven therapies, basic principles of cell therapy, and publishing responsibility.

Place, publisher, year, edition, pages
SAGE PUBLICATIONS INC, 2018
Keywords
cell therapy, neurorestoration, clinical application guideline neurorestoratology
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-357188 (URN)10.1177/0963689717746999 (DOI)000430019200009 ()29637817 (PubMedID)
Available from: 2018-08-13 Created: 2018-08-13 Last updated: 2018-08-13Bibliographically approved
Sharma, H. S., Muresanu, D. F., Vicente Lafuente, J., Patnaik, R., Tian, Z. R., Ozkizilcik, A., . . . Sharma, A. (2018). Co-Administration of TiO2 Nanowired Mesenchymal Stem Cells with Cerebrolysin Potentiates Neprilysin Level and Reduces Brain Pathology in Alzheimer's Disease. Molecular Neurobiology, 55(1), 300-311
Open this publication in new window or tab >>Co-Administration of TiO2 Nanowired Mesenchymal Stem Cells with Cerebrolysin Potentiates Neprilysin Level and Reduces Brain Pathology in Alzheimer's Disease
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 300-311Article in journal (Refereed) Published
Abstract [en]

Neprilysin (NPL), the rate-limiting enzyme for amyloid beta peptide (A beta P), appears to play a crucial role in the pathogenesis of Alzheimer's disease (AD). Since mesenchymal stem cells (MSCs) and/or cerebrolysin (CBL, a combination of neurotrophic factors and active peptide fragments) have neuroprotective effects in various CNS disorders, we examined nanowired delivery of MSCs and CBL on NPL content and brain pathology in AD using a rat model. AD-like symptoms were produced by intraventricular (i.c.v.) administration of A beta P (1-40) in the left lateral ventricle (250 ng/10 mu l, once daily) for 4 weeks. After 30 days, the rats were examined for NPL and A beta P concentrations in the brain and related pathology. Co-administration of TiO2-nanowired MSCs (10(6) cells) with 2.5 ml/kg CBL (i.v.) once daily for 1 week after 2 weeks of A beta P infusion significantly increased the NPL in the hippocampus (400 pg/g) from the untreated control group (120 pg/g; control 420 +/- 8 pg/g brain) along with a significant decrease in the A beta P deposition (45 pg/g from untreated control 75 pg/g; saline control 40 +/- 4 pg/g). Interestingly, these changes were much less evident when the MSCs or CBL treatment was given alone. Neuronal damages, gliosis, and myelin vesiculation were also markedly reduced by the combined treatment of TiO2, MSCs, and CBL in AD. These observations are the first to show that co-administration of TiO2-nanowired CBL and MSCs has superior neuroprotective effects in AD probably due to increasing the brain NPL level effectively, not reported earlier.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
Alzheimer's disease (AD), Neprilysin (NPL), Amyloid-beta peptide (a beta P), Mesenchymal stem cells (MSCs), Cerebrolysin (CBL), TiO2 nanowires, Nanodelivery
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-346902 (URN)10.1007/s12035-017-0742-9 (DOI)000424702600030 ()28844104 (PubMedID)
Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-04-04Bibliographically approved
Sharma, A., Muresanu, D. F., Vicente Lafuente, J., Sjöquist, P.-O., Patnaik, R., Tian, Z. R., . . . Sharma, H. S. (2018). Cold Environment Exacerbates Brain Pathology and Oxidative Stress Following Traumatic Brain Injuries: Potential Therapeutic Effects of Nanowired Antioxidant Compound H-290/51. Molecular Neurobiology, 55(1), 276-285
Open this publication in new window or tab >>Cold Environment Exacerbates Brain Pathology and Oxidative Stress Following Traumatic Brain Injuries: Potential Therapeutic Effects of Nanowired Antioxidant Compound H-290/51
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 276-285Article in journal (Refereed) Published
Abstract [en]

The possibility that traumatic brain injury (TBI) occurring in a cold environment exacerbates brain pathology and oxidative stress was examined in our rat model. TBI was inflicted by making a longitudinal incision into the right parietal cerebral cortex (2 mm deep and 4 mm long) in cold-acclimatized rats (5 degrees C for 3 h daily for 5 weeks) or animals at room temperature under Equithesin anesthesia. TBI in cold-exposed rats exhibited pronounced increase in brain lucigenin (LCG), luminol (LUM), and malondialdehyde (MDA) and marked pronounced decrease in glutathione (GTH) as compared to identical TBI at room temperature. The magnitude and intensity of BBB breakdown to radioiodine and Evans blue albumin, edema formation, and neuronal injuries were also exacerbated in cold-exposed rats after injury as compared to room temperature. Nanowired delivery of H-290/51 (50 mg/kg) 6 and 8 h after injury in cold-exposed group significantly thwarted brain pathology and oxidative stress whereas normal delivery of H-290/51 was neuroprotective after TBI at room temperature only. These observations are the first to demonstrate that (i) cold aggravates the pathophysiology of TBI possibly due to an enhanced production of oxidative stress, (ii) and in such conditions, nanodelivery of antioxidant compound has superior neuroprotective effects, not reported earlier.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
Traumatic brain injury (TBI), Oxidative stress, Luminol, Lucigenin, Malondialdehyde, Glutathione, H-290/51, Nanodelivery, Blood-brain barrier, Brain edema, Neuronal damage, Cold environment
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-346900 (URN)10.1007/s12035-017-0740-y (DOI)000424702600028 ()28856566 (PubMedID)
Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-04-04Bibliographically approved
Yang, H., Yang, Y., Qu, S., Wang, Z., Lu, W., Liu, F., . . . Luan, Z. (2018). Growth Factor Changes in Cerebrospinal Fluid of Children with Mental Retardation before and after Neural Precursor Cell Transplantation. CNS & Neurological Disorders: Drug Targets, 17(2), 98-105
Open this publication in new window or tab >>Growth Factor Changes in Cerebrospinal Fluid of Children with Mental Retardation before and after Neural Precursor Cell Transplantation
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2018 (English)In: CNS & Neurological Disorders: Drug Targets, ISSN 1871-5273, E-ISSN 1996-3181, Vol. 17, no 2, p. 98-105Article in journal (Refereed) Published
Abstract [en]

Objective: To investigate growth factor changes in cerebrospinal fluid (CSF) of children with mental retardation (MR) before and after neural precursor cell transplantation (NPCT), in an attempt to provide experimental support for the clinical treatment of MR with NPCT.

Methods: The study comprised of 28 MR children who received twice NPCT in our hospital. CSF was collected at both times of NPCT to assess growth factors by ELISA. In addition, the content of insulin-like growth factor 1 (IGF-1) in CSF was assayed to determine possible correlations between IGF-1 changes and the short-term therapeutic effect of NPCT.

Results: Of all the growth factors detected in CSF, only IGF-1 was increased significantly after NPCT (P<0.05). Fifteen of the twenty-eight MR children achieved short-term therapeutic efficacy, whereby the content of IGF-1 after NPCT was significantly higher than that before NPCT (P<0.05). There was no difference in IGF-1 content before and after NPCT in the remaining 13 MR children without short-term therapeutic effect (P=0.657). There was a significant difference in IGF-change between the two groups of patients (P<0.05).

Conclusion: IGF-1 may be one of the mechanisms contributing to the therapeutic effect of NPCT.

Place, publisher, year, edition, pages
BENTHAM SCIENCE PUBL, 2018
Keywords
Mental retardation, neural precursor cell, transplantation, insulin-like growth factor 1, growth factors, intellectual disability
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-359677 (URN)10.2174/1871527317666180411102337 (DOI)000435906600004 ()29637872 (PubMedID)
Funder
Swedish Research Council, 2710
Available from: 2018-09-06 Created: 2018-09-06 Last updated: 2018-09-06Bibliographically approved
Patnaik, R., Sharma, A., Skaper, S. D., Muresanu, D. F., Vicente Lafuente, J., Castellani, R. J., . . . Sharma, H. S. (2018). Histamine H3 Inverse Agonist BF 2649 or Antagonist with Partial H4 Agonist Activity Clobenpropit Reduces Amyloid Beta Peptide-Induced Brain Pathology in Alzheimer's Disease. Molecular Neurobiology, 55(1), 312-321
Open this publication in new window or tab >>Histamine H3 Inverse Agonist BF 2649 or Antagonist with Partial H4 Agonist Activity Clobenpropit Reduces Amyloid Beta Peptide-Induced Brain Pathology in Alzheimer's Disease
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 312-321Article in journal (Refereed) Published
Abstract [en]

Alzheimer's disease (AD) is one of the leading causes for disability and death affecting millions of people worldwide. Thus, novel therapeutic strategies are needed to reduce brain pathology associated with AD. In view of increasing awareness regarding involvement of histaminergic pathways in AD, we explored the role of one H3 receptor inverse agonist BF 2649 and one selective H3 receptor antagonist with partial H4 agonist activity in amyloid beta peptide (A beta P) infusion-induced brain pathology in a rat model. AD-like pathology was produced by administering A beta P (1-40) intracerebroventricular (i.c.v.) in the left lateral ventricle (250 ng/10 mu l, once daily) for 4 weeks. Control rats received saline. In separate group of rats, either BF 2649 (1 mg/kg, i.p.) or clobenpropit (1 mg/kg, i.p.) was administered once daily for 1 week after 3weeks of A beta P administration. After 30 days, blood-brain barrier (BBB) breakdown, edema formation, neuronal, glial injuries, and A beta P deposits were examined in the brain. A significant reduction in A beta P deposits along with marked reduction in neuronal or glial reactions was seen in the drug-treated group. The BBB breakdown to Evans blue albumin and radioiodine in the cortex, hippocampus, hypothalamus, and cerebellum was also significantly reduced in these drug-treated groups. Clobenpropit showed superior effects than the BF2649 in reducing brain pathology in AD. Taken together, our observations are the first to show that blockade of H3 and stimulation of H4 receptors are beneficial for the treatment of AD pathology, not reported earlier.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
Alzheimer's disease (AD). Histamine. Amyloid beta peptide (A beta P), Clobenpropit, BF2649, H3 receptor inverse agonist, H3 receptors antagonist with partial H4 agonist, Blood-brain barrier, Brain pathology
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-346903 (URN)10.1007/s12035-017-0743-8 (DOI)000424702600031 ()28861757 (PubMedID)
Available from: 2018-03-27 Created: 2018-03-27 Last updated: 2018-03-27Bibliographically approved
Requejo, C., Ruiz-Ortega, J. A., Cepeda, H., Sharma, A., Sharma, H., Ozkizilcik, A., . . . Lafuente, J. V. (2018). Nanodelivery of Cerebrolysin and Rearing in Enriched Environment Induce Neuroprotective Effects in a Preclinical Rat Model of Parkinson's Disease. Molecular Neurobiology, 55(1), 286-299
Open this publication in new window or tab >>Nanodelivery of Cerebrolysin and Rearing in Enriched Environment Induce Neuroprotective Effects in a Preclinical Rat Model of Parkinson's Disease
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 286-299Article in journal (Refereed) Published
Abstract [en]

Rearing in enriched environment (EE) improves the recuperation in animal models of Parkinson's disease (PD). Administration of TiO2-nanowired cerebrolysin (CBL) could represent an additional strategy to protect or repair the nigrostriatal system. This study aims to explore morphofunctional and biochemical changes in a preclinical stage of PD testing the synergistic efficiency of combining both strategies, housing in EE, and nanodelivery of CBL. Sprague-Dawley male rats receiving intrastriatally 6-hydroxydopamine after a short evolution time were segregated into CBL group (rats receiving nanowired CBL), EE group (rats housed in EE), CBL + EE group (rats housed in EE and receiving nanowired CBL), and control group (rats without additional treatment). Prodromic stage and treatment effects were characterized by the presence of motor symptoms (amphetamine-induced rotational behavior test). Tyrosine hydroxylase (TH) immunohistochemistry and Western blot (p-Akt/Akt and p-ERK/ERK 1/2 as survival markers and caspase-3 as apoptotic marker) were performed in striatum and SN. A decrease in motor symptoms was shown by rats receiving CBL. EE monitoring cages revealed that rats from CBL + EE group showed more significant number of laps in the wheel than EE group. In SN, CBL + EE group also presented the highest neuronal density. Moreover, p-Akt/Akt and p-ERK/ERK 1/2 ratio was significant higher and caspase-3 expression was lower in CBL + EE group. In conclusion, the combination of CBL and EE provided evidence of neuoprotective-neurorestorative mechanisms by which this combined strategy promoted morphofunctional improvement by activation of survival pathways after dopamine depletion in a preclinical model of PD.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
Parkinson'sdisease, 6-OHDA, Preclinical stage, Nanowired cerebrolysin, Enriched environment, Neuroprotection
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-346901 (URN)10.1007/s12035-017-0741-x (DOI)000424702600029 ()28840482 (PubMedID)
Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-04-04Bibliographically approved
Ozkizilcik, A., Sharma, A., Muresanu, D. F., Lafuente, J. V., Tian, Z. R., Patnaik, R., . . . Sharma, H. S. (2018). Timed Release of Cerebrolysin Using Drug-Loaded Titanate Nanospheres Reduces Brain Pathology and Improves Behavioral Functions in Parkinson's Disease. Molecular Neurobiology, 55(1), 359-369
Open this publication in new window or tab >>Timed Release of Cerebrolysin Using Drug-Loaded Titanate Nanospheres Reduces Brain Pathology and Improves Behavioral Functions in Parkinson's Disease
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 359-369Article in journal (Refereed) Published
Abstract [en]

Previous studies from our laboratory show that intraperitoneal injections of 1-metyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP, 20 mg/kg) daily within 2-h intervals for 5 days in mice induce Parkinson's disease (PD)-like symptoms on the 8th day. A significant decrease in dopamine (DA) and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) along with a marked decrease in the number of tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta (SNpc) and striatum (STr) confirms the validity of this model for studying PD. Since cerebrolysin (CBL) is a well-balanced composition of several neurotrophic factors and active peptide fragments, in the present investigation we examined the timed release of CBL using titanate nanospheres (TiNS) in treating PD in our mouse model. Our observations show that TiNS-CBL (in a dose of 3 ml/kg, i.v.) given after 2 days of MPTP administration for 5 days resulted in a marked increase in TH-positive cells in the SNpc and STr as compared to normal CBL. Also, TiNS-CBL resulted in significantly higher levels of DA, DOPAC, and HVA in SNpc and STr on the 8th day as compared to normal CBL therapy. TiNS-CBL also thwarted increased alpha-synuclein levels in the brain and in the cerebrospinal fluid (CSF) as well as neuronal nitric oxide synthase (nNOS) in the in PD brain as compared to untreated group. Behavioral function was also significantly improved in MPTP-treated animals that received TiNS-CBL. These observations are the first to demonstrate that timed release of TiNS-CBL has far more superior neuroprotective effects in PD than normal CBL.

Place, publisher, year, edition, pages
HUMANA PRESS INC, 2018
Keywords
1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridin (MPTP), Parkinson's disease (PD), Titanate nanospheres (TiNS), Cerebrolysin, Neuroprotection, Alpha-synuclein, Neuronal nitoic oxide synthase (nNOS), Cerebrospinal fluid (CSF)
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-347258 (URN)10.1007/s12035-017-0747-4 (DOI)000424702600035 ()28875428 (PubMedID)
Funder
Swedish Research Council, 2710-HSSGöran Gustafsson Foundation for Research in Natural Sciences and MedicineAstraZeneca
Available from: 2018-04-03 Created: 2018-04-03 Last updated: 2018-04-03Bibliographically approved
Feng, L., Sharma, A., Niu, F., Huang, Y., Vicente Lafuente, J., Muresanu, D. F., . . . Sharma, H. S. (2018). TiO2-Nanowired Delivery of DL-3-n-butylphthalide (DL-NBP) Attenuates Blood-Brain Barrier Disruption, Brain Edema Formation, and Neuronal Damages Following Concussive Head Injury. Molecular Neurobiology, 55(1), 350-358
Open this publication in new window or tab >>TiO2-Nanowired Delivery of DL-3-n-butylphthalide (DL-NBP) Attenuates Blood-Brain Barrier Disruption, Brain Edema Formation, and Neuronal Damages Following Concussive Head Injury
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2018 (English)In: Molecular Neurobiology, ISSN 0893-7648, E-ISSN 1559-1182, Vol. 55, no 1, p. 350-358Article in journal (Refereed) Published
Abstract [en]

DL-3-n-butylphthalide (DL-NBP) is one of the constituents of Chinese celery extract that is used to treat stroke, dementia, and ischemic diseases. However, its role in traumatic brain injury is less well known. In this investigation, neuroprotective effects of DL-NBP in concussive head injury (CHI) on brain pathology were explored in a rat model. CHI was inflicted in anesthetized rats by dropping a weight of 114.6 g from a height of 20 cm through a guide tube on the exposed right parietal bone inducing an impact of 0.224 N and allowed them to survive 4 to 24 h after the primary insult. DL-NBP was administered (40 or 60 mg/kg, i.p.) 2 and 4 h after injury in 8-h survival group and 8 and 12 h after trauma in 24-h survival group. In addition, TiO2-nanowired delivery of DL-NBP (20 or 40 mg/kg, i.p.) in 8 and 24 h CHI rats was also examined. Untreated CHI showed a progressive increase in blood-brain barrier (BBB) breakdown to Evans blue albumin (EBA) and radioiodine (I[131]-), edema formation, and neuronal injuries. The magnitude and intensity of these pathological changes were most marked in the left hemisphere. Treatment with DL-NBP significantly reduced brain pathology in CHI following 8 to 12 h at 40-mg dose. However, 60-mg dose is needed to thwart brain pathology at 24 h following CHI. On the other hand, TiO2-DL-NBP was effective in reducing brain damage up to 8 or 12 h using a 20-mg dose and only 40-mg dose was needed for neuroprotection in CHI at 24 h. These observations are the first to suggest that (i) DL-NBP is quite effective in reducing brain pathology and (ii) nanodelivery of DL-NBP has far more superior effects in CHI, not reported earlier.

Place, publisher, year, edition, pages
Humana Press, 2018
Keywords
DL-3-n-butylphthalide (DL-NBP), Concussive head injury (CHI), Blood-brain barrier, Brain edema, Neuronal injury, TiO2 nanodelivery, Neuroprotection
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-346905 (URN)10.1007/s12035-017-0746-5 (DOI)000424702600034 ()28856586 (PubMedID)
Available from: 2018-03-22 Created: 2018-03-22 Last updated: 2018-03-22Bibliographically approved
Sharma, H. S., Skaper, S. D. & Sharma, A. (2017). 10th Clinical Trials on Alzheimer's Disease (CTAD), Boston MA, USA, November 1-4, 2017. CNS & Neurological Disorders: Drug Targets, 16(10), 1134-1137
Open this publication in new window or tab >>10th Clinical Trials on Alzheimer's Disease (CTAD), Boston MA, USA, November 1-4, 2017
2017 (English)In: CNS & Neurological Disorders: Drug Targets, ISSN 1871-5273, E-ISSN 1996-3181, Vol. 16, no 10, p. 1134-1137Article in journal, Editorial material (Other academic) Published
Place, publisher, year, edition, pages
BENTHAM SCIENCE PUBL, 2017
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-356918 (URN)10.2174/187152731610180313114311 (DOI)000428516200011 ()29583111 (PubMedID)
Available from: 2018-08-09 Created: 2018-08-09 Last updated: 2018-08-09Bibliographically approved
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