title: (-)-Epigallocatechin-3-gallate (EGCG) attenuates functional deficits and morphological alterations by diminishing apoptotic gene overexpression in skeletal muscles after sciatic nerve crush injury.
abstract: Muscle degeneration and impairment following nerve injury could lead to apoptosis as a result of increased levels of reactive oxygen species. This activates the apoptotic cascade through mitochondrial dysfunction and damage to lipids, proteins, and DNA. In considering of the multifactorial protective properties of green tea polyphenols (-)-epigallocatechin-3-gallate (EGCG), this study investigates whether EGCG treatment does improve skeletal muscle function impairments, induced by crushing of the sciatic nerve. Compared to the saline-treated injured group of animals, EGCG treatment of axonotomized animals showed significant motor enhancement in the toe spread and foot positioning analysis and gain in the percentage motor deficit. The proprioceptive function expressed by the hopping response showed significant progression in the EGCG-treated group. Recovery of sensory innervation was followed by a slowly retreating neuropathic pain-like syndrome in the EGCG-treated animals. Muscle tissues from injured limb showed severe histopathological alterations that were significantly attenuated by EGCG treatment at the end of week 3 post-surgery. Semi-quantitative desmin immunohistochemistry revealed intense staining in the saline-treated injured animals, whereas EGCG treatment decreased the desmin immunoreactivity back to sham control levels. Using RT-PCR, EGCG treatment induced a significant anti-apoptotic effect in injured muscle tissues by normalizing the Bax/Bcl-2 ratio back to baseline levels and inhibiting overexpression of the p53 apoptotic gene at days 3 and 7 post-surgery. In conclusion, our results demonstrate that EGCG enhances functional recovery, protects muscle fibers from cellular death by activating anti-apoptotic signaling pathway, and improves morphological recovery in skeletal muscle after nerve injuries.
authors.affiliation: Department of Anatomy, Faculty of Medicine, Kuwait University, PO Box 24923, Safat 13110, Kuwait. wrenno@hsc.edu.kw
authors.forename: Waleed M
authors.initials: WM
authors.lastname: Renno
authors.forename: May
authors.initials: M
authors.lastname: Al-Maghrebi
authors.forename: Anwar
authors.initials: A
authors.lastname: Al-Banaw
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis* / Q000235:genetics*; D001522:Behavior, Animal / Q000187:drug effects; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D003893:Desmin / Q000378:metabolism; D005528:Foot / Q000502:physiology; D006358:Hot Temperature; D006930:Hyperalgesia / Q000188:drug therapy / Q000209:etiology; D007150:Immunohistochemistry; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000473:pathology; D009409:Nerve Crush; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010147:Pain Measurement / Q000187:drug effects; D011187:Posture / Q000502:physiology; D012313:RNA / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects; D060888:Real-Time Polymerase Chain Reaction; D020127:Recovery of Function; D020426:Sciatic Neuropathy / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects; D014034:Toes / Q000502:physiology
chemical_list: D051017:Apoptosis Regulatory Proteins; D003893:Desmin; D018696:Neuroprotective Agents; D012313:RNA; D002392:Catechin; C045651:epigallocatechin gallate