G
Goldy
Guest
I ran across this on another board and along with muscle tissue accrual is one of the main reasons I use low dose clen (40 mcg eod), as a couple of years ago I had major issues with sciatica which is now completely cured since I began the clen therapy:
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Regeneration of peripheral nerves after clenbuterol treatment in a rat model.
Frerichs O, Fansa H, Ziems P, Schneider W, Keilhoff G.
Department of Plastic, Reconstructive, and Hand Surgery, Otto-von-Guericke University, Leipziger Str. 44, 39120 Magdeburg, Germany. onno.frerichs@medizin.uni-magdeburg.de
Abstract
Clenbuterol is known to act as a neuroprotective substance in the central nervous system, and also reduces muscle atrophy after denervation. The aim of this study was to evaluate its influence on peripheral nerve regeneration. The rat sciatic nerve model was used in four groups (n = 8 per group). After complete nerve transection and microsurgical coaptation, two groups received a daily oral dose of 100 microg/kg clenbuterol and two served as controls. Regeneration was assessed clinically, histologically, and morphometrically after 4 and 6 weeks. The weight ratios of calf muscles were calculated. Histological examination showed significantly increased axon counts in the clenbuterol group and a better degree of myelination. Muscle weight ratios of the clenbuterol group were significantly increased after 6 weeks, and the animals showed improved function of the hindlimb. Thus, therapy with 100 microg/kg clenbuterol daily after coaptation of a sciatic nerve showed a positive influence on clinical, histological, and morphometrical parameters in the rat model. The underlying mechanism remains unclear.
Copyright 2001 John Wiley & Sons, Inc.
http://www.ncbi.nlm.nih.gov/pubmed/11745978
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The influence on nerve regeneration by the beta2-receptor agonist clenbuterol
[Article in German]
Frerichs O, Fansa H, Ziems P, Keilhoff G, Schneider W.
Klinik für Plastische, Wiederherstellungs- und Handchirurgie, Otto-von-Guericke-Universität Magdeburg, Germany. Onno.Frerichs@medizin.uni-magdeburg.de
Abstract
PURPOSE: Clenbuterol has shown a neuroprotective action in the central nervous system by induction of growth factors after cellular damage. Additionally, the atrophy of sceletal muscle is attenuated by the application of Clenbuterol after denervation. This experiment was performed to show the influence of Clenbuterol on regeneration of peripheral nerves. MEHOD AND MATERIAL: In a rat model, the sciatic nerve was transected and microsurgically coaptated. Eight animals in each group received a daily oral dosage of 100 microg/kg bodyweight during four, respectively six weeks. Two control groups received only drinking water under the otherwise same protocol. The assessment was done histologically, morphometrically and clinically. The weight ratio of the soleus and extensor digitorum muscles of the operated to the contralateral side was measured.
RESULTS: The groups treated with Clenbuterol showed histologically and morphometrically a significantly increased axon count and a better g-ratio. The muscle weight ratio was significantly higher in the Clenbuterol group after six weeks and more animals in this group were able to spread their toes.
CONCLUSION: The oral application of Clenbuterol in a rodent model shows a positive influence on nerve regeneration.
http://www.ncbi.nlm.nih.gov/pubmed/12073183
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Partial functional recovery after complete spinal cord transection by combined chondroitinase and clenbuterol treatment.
Bai F, Peng H, Etlinger JD, Zeman RJ.
Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595, USA.
Abstract
Spinal cord injury not only disrupts axonal tracts but also causes gliotic, fibrotic, and Schwannotic scarring with resulting deposition of chondroitin sulfate proteoglycans (CSPGs) which prevent axonal reconnection and recovery of locomotor function. Here, we determined whether recovery of locomotor function could be promoted after complete transection, by degrading CSPGs enzymatically within the injury site with chondroitinase ABC (chABC) together with treatment with the beta(2)-adrenoceptor agonist, clenbuterol, a neuroprotective agent which can promote regrowth of lower motoneurons. Partial recovery of locomotor function was observed 8-12 weeks postinjury only after combined chABC and clenbuterol treatment. The recovery of locomotor function coincided with the presence of axons caudal to the injury site arising from neurons of the reticular, vestibular, and red nuclei also only with combined chABC and clenbuterol treatment. Axons myelinated by Schwann cells were most prominent in the transection site in the combined treatment group. Clenbuterol treatment activated cAMP response element binding protein within retrogradely traced neurons which has been associated with axonal regrowth. ChABC treatment decreased scarring due to both CSPG and collagen deposition as well as the gap between intact regions of the spinal cord. ChABC also increased numbers of phagocytic cells which remove myelin debris as well as populations of astrocytes thereby aiding blood-spinal cord barrier reformation. Together the results suggest that chABC and clenbuterol can act synergistically to promote recovery of locomotor function.
http://www.ncbi.nlm.nih.gov/pubmed/20552220
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.
.
"
Regeneration of peripheral nerves after clenbuterol treatment in a rat model.
Frerichs O, Fansa H, Ziems P, Schneider W, Keilhoff G.
Department of Plastic, Reconstructive, and Hand Surgery, Otto-von-Guericke University, Leipziger Str. 44, 39120 Magdeburg, Germany. onno.frerichs@medizin.uni-magdeburg.de
Abstract
Clenbuterol is known to act as a neuroprotective substance in the central nervous system, and also reduces muscle atrophy after denervation. The aim of this study was to evaluate its influence on peripheral nerve regeneration. The rat sciatic nerve model was used in four groups (n = 8 per group). After complete nerve transection and microsurgical coaptation, two groups received a daily oral dose of 100 microg/kg clenbuterol and two served as controls. Regeneration was assessed clinically, histologically, and morphometrically after 4 and 6 weeks. The weight ratios of calf muscles were calculated. Histological examination showed significantly increased axon counts in the clenbuterol group and a better degree of myelination. Muscle weight ratios of the clenbuterol group were significantly increased after 6 weeks, and the animals showed improved function of the hindlimb. Thus, therapy with 100 microg/kg clenbuterol daily after coaptation of a sciatic nerve showed a positive influence on clinical, histological, and morphometrical parameters in the rat model. The underlying mechanism remains unclear.
Copyright 2001 John Wiley & Sons, Inc.
http://www.ncbi.nlm.nih.gov/pubmed/11745978
--------------------
The influence on nerve regeneration by the beta2-receptor agonist clenbuterol
[Article in German]
Frerichs O, Fansa H, Ziems P, Keilhoff G, Schneider W.
Klinik für Plastische, Wiederherstellungs- und Handchirurgie, Otto-von-Guericke-Universität Magdeburg, Germany. Onno.Frerichs@medizin.uni-magdeburg.de
Abstract
PURPOSE: Clenbuterol has shown a neuroprotective action in the central nervous system by induction of growth factors after cellular damage. Additionally, the atrophy of sceletal muscle is attenuated by the application of Clenbuterol after denervation. This experiment was performed to show the influence of Clenbuterol on regeneration of peripheral nerves. MEHOD AND MATERIAL: In a rat model, the sciatic nerve was transected and microsurgically coaptated. Eight animals in each group received a daily oral dosage of 100 microg/kg bodyweight during four, respectively six weeks. Two control groups received only drinking water under the otherwise same protocol. The assessment was done histologically, morphometrically and clinically. The weight ratio of the soleus and extensor digitorum muscles of the operated to the contralateral side was measured.
RESULTS: The groups treated with Clenbuterol showed histologically and morphometrically a significantly increased axon count and a better g-ratio. The muscle weight ratio was significantly higher in the Clenbuterol group after six weeks and more animals in this group were able to spread their toes.
CONCLUSION: The oral application of Clenbuterol in a rodent model shows a positive influence on nerve regeneration.
http://www.ncbi.nlm.nih.gov/pubmed/12073183
-------------------------
Partial functional recovery after complete spinal cord transection by combined chondroitinase and clenbuterol treatment.
Bai F, Peng H, Etlinger JD, Zeman RJ.
Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595, USA.
Abstract
Spinal cord injury not only disrupts axonal tracts but also causes gliotic, fibrotic, and Schwannotic scarring with resulting deposition of chondroitin sulfate proteoglycans (CSPGs) which prevent axonal reconnection and recovery of locomotor function. Here, we determined whether recovery of locomotor function could be promoted after complete transection, by degrading CSPGs enzymatically within the injury site with chondroitinase ABC (chABC) together with treatment with the beta(2)-adrenoceptor agonist, clenbuterol, a neuroprotective agent which can promote regrowth of lower motoneurons. Partial recovery of locomotor function was observed 8-12 weeks postinjury only after combined chABC and clenbuterol treatment. The recovery of locomotor function coincided with the presence of axons caudal to the injury site arising from neurons of the reticular, vestibular, and red nuclei also only with combined chABC and clenbuterol treatment. Axons myelinated by Schwann cells were most prominent in the transection site in the combined treatment group. Clenbuterol treatment activated cAMP response element binding protein within retrogradely traced neurons which has been associated with axonal regrowth. ChABC treatment decreased scarring due to both CSPG and collagen deposition as well as the gap between intact regions of the spinal cord. ChABC also increased numbers of phagocytic cells which remove myelin debris as well as populations of astrocytes thereby aiding blood-spinal cord barrier reformation. Together the results suggest that chABC and clenbuterol can act synergistically to promote recovery of locomotor function.
http://www.ncbi.nlm.nih.gov/pubmed/20552220