Tags

Type your tag names separated by a space and hit enter

Hypoxic-conditioned medium from adipose tissue mesenchymal stem cells improved neuroinflammation through alternation of toll like receptor (TLR) 2 and TLR4 expression in model of Alzheimer's disease rats.
Behav Brain Res 2019; :112362BB

Abstract

Microglia have a pivotal role to initiate immune responses in AD brains through toll-like receptors and induce neuroinflammation. Adipose tissue mesenchymal stem cells (ATSCs) secret many neurotrophic and anti-inflammatory factors called conditioned medium (CM). Many studies have demonstrated that CM of mesenchymal stem cells facilitate regeneration and attenuates inflammation in many disorders. To this purpose, the effect of ATSCs-conditioned medium (ATSC-CM) on brain inflammation and the role of toll-like receptors were investigated in this study. Seventy-two rats were randomly divided into 6 groups: control, sham, sham+ATSC-CM: 200μl ATSC-CM once a day intraperitoneally for 8 days, AD group injected the Aβ1-40 intra-hippocampal, AD+ASC-CM, which was injected Aβ1-40 intra-hippocampal and 200μl ATSC-CM once a day intraperitoneally for 8 days and AD+ rivastigmine: was injected Aβ1-40 intra-hippocampal and received rivastigmine (0.6 mg/kg) orally once a day for 2 weeks. Memory and learning were measured by Morris water maze and novel object recognition tests. For detection of beta-amyloid plaque, Congo red staining was used, and neuronal survival was assessed by Nissl staining. Expression of TLR2 and TLR4 was measured by real-time PCR, and finally, to assess inflammation markers (IL-1β and TNF-α) in the hippocampus, ELISA kits were used. In treatment group spatial and recognition memory significantly was improved. ATSC-CM administration decreased beta amyloid plaques and enhanced neuronal survival in AD brain rats. In addition, TLR2 and TLR4 expression decreased in treatment group. Results also showed that ATSC-CM reduced IL-1β and TNF-α as inflammation markers. ATSC-CM improved memory deficit, decreased beta amyloids formation, increased neuron survival, and attenuated inflammation by reducing the expression of TLRs.

Authors+Show Affiliations

Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran; Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: shahabsadr2012@yahoo.com.Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Department of Nursing, Abadan Faculty of Medical Sciences, Abadan, Iran.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31739000

Citation

Mehrabadi, Shima, et al. "Hypoxic-conditioned Medium From Adipose Tissue Mesenchymal Stem Cells Improved Neuroinflammation Through Alternation of Toll Like Receptor (TLR) 2 and TLR4 Expression in Model of Alzheimer's Disease Rats." Behavioural Brain Research, 2019, p. 112362.
Mehrabadi S, Motevaseli E, Sadr SS, et al. Hypoxic-conditioned medium from adipose tissue mesenchymal stem cells improved neuroinflammation through alternation of toll like receptor (TLR) 2 and TLR4 expression in model of Alzheimer's disease rats. Behav Brain Res. 2019.
Mehrabadi, S., Motevaseli, E., Sadr, S. S., & Moradbeygi, K. (2019). Hypoxic-conditioned medium from adipose tissue mesenchymal stem cells improved neuroinflammation through alternation of toll like receptor (TLR) 2 and TLR4 expression in model of Alzheimer's disease rats. Behavioural Brain Research, p. 112362. doi:10.1016/j.bbr.2019.112362.
Mehrabadi S, et al. Hypoxic-conditioned Medium From Adipose Tissue Mesenchymal Stem Cells Improved Neuroinflammation Through Alternation of Toll Like Receptor (TLR) 2 and TLR4 Expression in Model of Alzheimer's Disease Rats. Behav Brain Res. 2019 Nov 15;112362. PubMed PMID: 31739000.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hypoxic-conditioned medium from adipose tissue mesenchymal stem cells improved neuroinflammation through alternation of toll like receptor (TLR) 2 and TLR4 expression in model of Alzheimer's disease rats. AU - Mehrabadi,Shima, AU - Motevaseli,Elahe, AU - Sadr,Seyed Shahabeddin, AU - Moradbeygi,Khadijeh, Y1 - 2019/11/15/ PY - 2019/09/30/received PY - 2019/11/11/revised PY - 2019/11/14/accepted PY - 2019/11/19/pubmed PY - 2019/11/19/medline PY - 2019/11/19/entrez KW - Alzheimer disease KW - Mesenchymal stem cell conditioned medium KW - Neuroinflammation KW - TLR2 KW - TLR4 SP - 112362 EP - 112362 JF - Behavioural brain research JO - Behav. Brain Res. N2 - Microglia have a pivotal role to initiate immune responses in AD brains through toll-like receptors and induce neuroinflammation. Adipose tissue mesenchymal stem cells (ATSCs) secret many neurotrophic and anti-inflammatory factors called conditioned medium (CM). Many studies have demonstrated that CM of mesenchymal stem cells facilitate regeneration and attenuates inflammation in many disorders. To this purpose, the effect of ATSCs-conditioned medium (ATSC-CM) on brain inflammation and the role of toll-like receptors were investigated in this study. Seventy-two rats were randomly divided into 6 groups: control, sham, sham+ATSC-CM: 200μl ATSC-CM once a day intraperitoneally for 8 days, AD group injected the Aβ1-40 intra-hippocampal, AD+ASC-CM, which was injected Aβ1-40 intra-hippocampal and 200μl ATSC-CM once a day intraperitoneally for 8 days and AD+ rivastigmine: was injected Aβ1-40 intra-hippocampal and received rivastigmine (0.6 mg/kg) orally once a day for 2 weeks. Memory and learning were measured by Morris water maze and novel object recognition tests. For detection of beta-amyloid plaque, Congo red staining was used, and neuronal survival was assessed by Nissl staining. Expression of TLR2 and TLR4 was measured by real-time PCR, and finally, to assess inflammation markers (IL-1β and TNF-α) in the hippocampus, ELISA kits were used. In treatment group spatial and recognition memory significantly was improved. ATSC-CM administration decreased beta amyloid plaques and enhanced neuronal survival in AD brain rats. In addition, TLR2 and TLR4 expression decreased in treatment group. Results also showed that ATSC-CM reduced IL-1β and TNF-α as inflammation markers. ATSC-CM improved memory deficit, decreased beta amyloids formation, increased neuron survival, and attenuated inflammation by reducing the expression of TLRs. SN - 1872-7549 UR - https://www.unboundmedicine.com/medline/citation/31739000/Hypoxic-Conditioned_Medium_from_Adipose_Tissue_Mesenchymal_Stem_Cells_Improved_Neuroinflammation_through_Alternation_of_Toll_like_receptor_(TLR)_2_and_TLR4_Expression_in_Model_of_Alzheimer's_Disease_Rats L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(19)31469-X DB - PRIME DP - Unbound Medicine ER -