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1.
Plast Reconstr Surg ; 148(6): 1357-1365, 2021 Dec 01.
Article in English | MEDLINE | ID: mdl-34705806

ABSTRACT

BACKGROUND: A commonly seen issue in facial palsy patients is brow ptosis caused by paralysis of the frontalis muscle powered by the frontal branch of the facial nerve. Predominantly, static methods are used for correction. Functional restoration concepts include the transfer of the deep temporal branch of the trigeminal nerve and cross-facial nerve grafts. Both techniques can neurotize the original mimic muscles in early cases or power muscle transplants in late cases. Because axonal capacity is particularly important in cross-facial nerve graft procedures, the authors investigated the microanatomical features of the frontal branch to provide the basis for its potential use and to ease intraoperative donor nerve selection. METHODS: Nerve biopsy specimens from 106 fresh-frozen cadaver facial halves were obtained. Histologic processing and digitalization were followed by nerve morphometric analysis and semiautomated axon quantification. RESULTS: The frontal branch showed a median of three fascicles (n = 100; range, one to nine fascicles). A mean axonal capacity of 1191 ± 668 axons (range, 186 to 3539 axons; n = 88) and an average cross-sectional diameter of 1.01 ± 0.26 mm (range, 0.43 to 1.74 mm; n = 67) were noted. In the linear regression model, diameter and axonal capacity demonstrated a positive relation (n = 57; r2 = 0.32; p < 0.001). Based on that equation, a nerve measuring 1 mm is expected to carry 1339 axons. CONCLUSION: The authors' analysis on the microanatomy of the frontal branch could promote clinical use of cross-facial nerve graft procedures in frontalis muscle neurotization and free muscle transplantations.


Subject(s)
Facial Muscles/innervation , Facial Nerve/anatomy & histology , Facial Paralysis/surgery , Nerve Transfer/methods , Aged , Aged, 80 and over , Axons/physiology , Cadaver , Facial Nerve/physiopathology , Facial Nerve/surgery , Facial Nerve/transplantation , Facial Paralysis/physiopathology , Female , Humans , Male , Nerve Regeneration/physiology
2.
J Biol Chem ; 286(8): 5942-55, 2011 Feb 25.
Article in English | MEDLINE | ID: mdl-21169355

ABSTRACT

Recent studies have demonstrated that transcription factor nuclear factor (NF)-κB inhibition may contribute to the protective anti-inflammatory actions of andrographolide, an abundant component of plants of the genus Andrographis. However, the precise mechanism by which andrographolide inhibits NF-κB signaling remains unclear. We thus investigated the mechanism involved in andrographolide suppression of NF-κB signaling in rat vascular smooth muscle cells (VSMCs) exposed to proinflammatory stimuli, LPS, and IFN-γ. Andrographolide was shown to suppress LPS/IFN-γ-induced inducible nitric-oxide synthase and matrix metalloprotease 9 expression in rat VSMCs. Andrographolide also inhibited LPS/IFN-γ-induced p65 nuclear translocation, DNA binding activity, p65 Ser(536) phosphorylation, and NF-κB reporter activity. However, IKK phosphorylation and downstream inhibitory κBα phosphorylation and degradation were not altered by the presence of andrographolide in LPS/IFN-γ-stimulated VSMCs. These andrographolide inhibitory actions could be prevented by selective inhibition of neutral sphingomyelinase and protein phosphatase 2A (PP2A). Furthermore, andrographolide was demonstrated to increase ceramide formation and PP2A activity in VSMCs and to inhibit neointimal formation in rat carotid injury models. These results suggest that andrographolide caused neutral sphingomyelinase-mediated ceramide formation and PP2A activation to dephosphorylate p65 Ser(536), leading to NF-κB inactivation and subsequent inducible nitric-oxide synthase down-regulation in rat VSMCs stimulated by LPS and IFN-γ.


Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Cell Nucleus/metabolism , Diterpenes/pharmacology , Muscle, Smooth, Vascular/metabolism , Myocytes, Smooth Muscle/metabolism , Protein Phosphatase 2/metabolism , Transcription Factor RelA/metabolism , Active Transport, Cell Nucleus/drug effects , Andrographis/chemistry , Animals , Anti-Inflammatory Agents, Non-Steroidal/chemistry , Ceramides/metabolism , Diterpenes/chemistry , Enzyme Activation/drug effects , Interferon-gamma/pharmacology , Lipopolysaccharides/pharmacology , Male , Matrix Metalloproteinase 9/biosynthesis , Muscle, Smooth, Vascular/cytology , Myocytes, Smooth Muscle/cytology , Nitric Oxide Synthase Type II/biosynthesis , Phosphorylation/drug effects , Rats , Rats, Wistar , Serine/metabolism , Sphingomyelin Phosphodiesterase/antagonists & inhibitors , Sphingomyelin Phosphodiesterase/metabolism
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