title: Nanolipodendrosome-loaded glatiramer acetate and myogenic differentiation 1 as augmentation therapeutic strategy approaches in muscular dystrophy.
abstract: BACKGROUND
  [Corrected] Muscular dystrophies consist of a number of juvenile and adult forms of complex disorders which generally cause weakness or efficiency defects affecting skeletal muscles or, in some kinds, other types of tissues in all parts of the body are vastly affected. In previous studies, it was observed that along with muscular dystrophy, immune inflammation was caused by inflammatory cells invasion - like T lymphocyte markers (CD8+/CD4+). Inflammatory processes play a major part in muscular fibrosis in muscular dystrophy patients. Additionally, a significant decrease in amounts of two myogenic recovery factors (myogenic differentation 1 [MyoD] and myogenin) in animal models was observed. The drug glatiramer acetate causes anti-inflammatory cytokines to increase and T helper (Th) cells to induce, in an as yet unknown mechanism. MyoD recovery activity in muscular cells justifies using it alongside this drug.
  
  
  METHODS
  In this study, a nanolipodendrosome carrier as a drug delivery system was designed. The purpose of the system was to maximize the delivery and efficiency of the two drug factors, MyoD and myogenin, and introduce them as novel therapeutic agents in muscular dystrophy phenotypic mice. The generation of new muscular cells was analyzed in SW1 mice. Then, immune system changes and probable side effects after injecting the nanodrug formulations were investigated.
  
  
  RESULTS
  The loaded lipodendrimer nanocarrier with the candidate drug, in comparison with the nandrolone control drug, caused a significant increase in muscular mass, a reduction in CD4+/CD8+ inflammation markers, and no significant toxicity was observed. The results support the hypothesis that the nanolipodendrimer containing the two candidate drugs will probably be an efficient means to ameliorate muscular degeneration, and warrants further investigation.
authors: Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
authors: Ehsan
authors: E
authors: Afzal
authors: Saba
authors: S
authors: Zakeri
authors: Peyman
authors: P
authors: Keyhanvar
authors: Meisam
authors: M
authors: Bagheri
authors: Parvin
authors: P
authors: Mahjoubi
authors: Mahtab
authors: M
authors: Asadian
authors: Nogol
authors: N
authors: Omoomi
authors: Mohammad
authors: M
authors: Dehqanian
authors: Negar
authors: N
authors: Ghalandarlaki
authors: Tahmineh
authors: T
authors: Darvishmohammadi
authors: Fatemeh
authors: F
authors: Farjadian
authors: Mohammad Sadegh
authors: MS
authors: Golvajoee
authors: Shadi
authors: S
authors: Afzal
authors: Maryam
authors: M
authors: Ghaffari
authors: Reza Ahangari
authors: RA
authors: Cohan
authors: Amin
authors: A
authors: Gravand
authors: Mehdi Shafiee
authors: MS
authors: Ardestani
mesh_terms: D000818:Animals; D001835:Body Weight / Q000187:drug effects; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D000068717:Glatiramer Acetate; D008081:Liposomes / Q000737:chemistry / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D046529:Microscopy, Electron, Transmission; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology; D009136:Muscular Dystrophies / Q000188:drug therapy*; D017570:MyoD Protein / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*; D009277:Nandrolone / Q000494:pharmacology; D053758:Nanoparticles / Q000737:chemistry / Q000627:therapeutic use*; D010316:Particle Size; D010455:Peptides / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D008081:Liposomes; D017570:MyoD Protein; C057363:MyoD1 myogenic differentiation protein; D010455:Peptides; D000068717:Glatiramer Acetate; D009277:Nandrolone
keywords: MyoD factor; drug delivery; glatiramer acetate; muscular dystrophy
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