title: (-)-Epigallocatechin-3-gallate modulates spinal cord neuronal degeneration by enhancing growth-associated protein 43, B-cell lymphoma 2, and decreasing B-cell lymphoma 2-associated x protein expression after sciatic nerve crush injury.
abstract: Our previous studies have established that (-)-epigallocatechin-3-gallate (EGCG) has both neuroprotective and -regenerative capacity after sciatic nerve injury. Moreover, this improvement was evident on the behavioral level. The aim of this study was to investigate the central effects of ECGC on spinal cord motor neurons after sciatic nerve injury. Our study showed that administering 50 mg/kg intraperitoneally i.p. of EGCG to sciatic nerve-injured rats improved their performance on different motor functions and mechanical hyperesthesia neurobehavioral tests. Histological analysis of spinal cords of EGCG-treated sciatic nerve-injured (CRUSH+ECGC) animals showed an increase in the number of neurons in the anterior horn, when compared to the naïve, sham, and saline-treated sciatic nerve-injured (CRUSH) control groups. Additionally, immunohistochemical study of spinal cord sections revealed that EGCG reduced the expression of glial fibrillary acidic protein and increased the expression of growth-associated protein 43, a marker of regenerating axons. Finally, EGCG reduced the ratio of B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 and increased the expression of survivin gene. This study may shed some light on the future clinical use of EGCG and its constituents in the treatment of peripheral nerve injury.
authors.affiliation: 1 Department of Anatomy, Faculty of Medicine, Kuwait University , Safat, Kuwait .
authors.forename: Waleed M
authors.initials: WM
authors.lastname: Renno
authors.forename: May
authors.initials: M
authors.lastname: Al-Maghrebi
authors.forename: Muddanna S
authors.initials: MS
authors.lastname: Rao
authors.forename: Haitham
authors.initials: H
authors.lastname: Khraishah
mesh_terms: D000818:Animals; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D004195:Disease Models, Animal; D019922:GAP-43 Protein / Q000096:biosynthesis; D007150:Immunohistochemistry; D008297:Male; D009409:Nerve Crush; D009410:Nerve Degeneration / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D059348:Peripheral Nerve Injuries / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D020127:Recovery of Function / Q000187:drug effects*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012584:Sciatic Nerve / Q000293:injuries; D013116:Spinal Cord / Q000187:drug effects* / Q000473:pathology; D051020:bcl-X Protein / Q000096:biosynthesis
chemical_list: C494813:Bcl2l1 protein, rat; D019922:GAP-43 Protein; D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051020:bcl-X Protein; D002392:Catechin; C045651:epigallocatechin gallate
keywords: apoptosis; green tea; neuroprotection; neuroregeneration; surviving