跳到主要內容

臺灣博碩士論文加值系統

(44.192.48.196) 您好!臺灣時間:2024/06/23 20:49
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果 :::

詳目顯示

: 
twitterline
研究生:Le Duc THinh
研究生(外文):Le Duc Thinh
論文名稱:低能雷射治療對糖尿病合併後肢缺血小鼠其肌肉萎縮的影響
論文名稱(外文):EFFECT OF LOW-LEVEL LASER THERAPY ON MUSCLE ATROPHY ON PERIPHERAL ARTERY DISEASE MICE WITH DIABETES
指導教授:鄭宇容鄭宇容引用關係
指導教授(外文):Yu-jung Cheng
學位類別:碩士
校院名稱:中國醫藥大學
系所名稱:物理治療學系復健科學碩士班
學門:醫藥衛生學門
學類:復健醫學學類
論文種類:學術論文
論文出版年:2020
畢業學年度:108
語文別:英文
論文頁數:44
中文關鍵詞:LaserDiabetesPADMuscle atrophyAngiogenesis
外文關鍵詞:LaserDiabetesPADMuscle atrophyAngiogenesis
相關次數:
  • 被引用被引用:0
  • 點閱點閱:86
  • 評分評分:
  • 下載下載:10
  • 收藏至我的研究室書目清單書目收藏:0
Background: Patients with diabetes mellitus (DM) are at high risk of peripheral arterial disease (PAD) in lower extremities, and it could cause muscle atrophy. Low-level laser therapy (LLLT) has shown beneficial effects on both damaged vascular and muscle condition, thus, the application of LLLT on muscle atrophy in the PAD mice model with DM was tested.
Methods: Thirty C57/BL6 mice were divided into 4 groups: control, LLLT, DM + LLLT, and DM; DM was induced by intraperitoneal injection with 50mg/kg streptozotocin. Left femoral artery ligation was performed later to mimic PAD. Animals then examined by LASER Doppler for blood perfusion before treated with Al-GaInP-diode laser, 660 nm wavelength, 3.18 mW/cm2 for 10 minutes, 7 sessions, a total of 15 days. After sacrificed, gastrocnemius muscles were collected, weighed, and analyzed with immunofluorescence of Collagen type IV. Protein extract was analyzed by Western blot for phospho-AKT/AKT, phospho-ERK/ERK, phospho-mTOR/mTOR; iNOS, and phospho-eNOS/eNOS, and VEGF ELISA.
Results: After LASER intervention, blood perfusion of the DM group was significantly lower than the DM + LLLT group and muscle weight of the diabetes group also has a statistically decrease compare to control and LLLT groups. Immunofluorescence staining showed a significant decrease in big-size muscle fibers numbers in DM group compared to DM + LLLT group. Western blot showed an increase in mTOR phosphorylation in DM + LLLT groups than the DM group. iNOS level of both DM groups was significantly lower than the control group, while eNOS activation in DM + LLLT group was higher than the control and LLLT group. ERK activation level in DM + LLLT group also significantly higher than the control group. In AKT phosphorylation and VEGF level, no statistical difference was found among groups.
Conclusions: The present results showed LLLT has a positive effect on PAD mice with DM, including increasing blood perfusion and preventing muscle atrophy
Background: Patients with diabetes mellitus (DM) are at high risk of peripheral arterial disease (PAD) in lower extremities, and it could cause muscle atrophy. Low-level laser therapy (LLLT) has shown beneficial effects on both damaged vascular and muscle condition, thus, the application of LLLT on muscle atrophy in the PAD mice model with DM was tested.
Methods: Thirty C57/BL6 mice were divided into 4 groups: control, LLLT, DM + LLLT, and DM; DM was induced by intraperitoneal injection with 50mg/kg streptozotocin. Left femoral artery ligation was performed later to mimic PAD. Animals then examined by LASER Doppler for blood perfusion before treated with Al-GaInP-diode laser, 660 nm wavelength, 3.18 mW/cm2 for 10 minutes, 7 sessions, a total of 15 days. After sacrificed, gastrocnemius muscles were collected, weighed, and analyzed with immunofluorescence of Collagen type IV. Protein extract was analyzed by Western blot for phospho-AKT/AKT, phospho-ERK/ERK, phospho-mTOR/mTOR; iNOS, and phospho-eNOS/eNOS, and VEGF ELISA.
Results: After LASER intervention, blood perfusion of the DM group was significantly lower than the DM + LLLT group and muscle weight of the diabetes group also has a statistically decrease compare to control and LLLT groups. Immunofluorescence staining showed a significant decrease in big-size muscle fibers numbers in DM group compared to DM + LLLT group. Western blot showed an increase in mTOR phosphorylation in DM + LLLT groups than the DM group. iNOS level of both DM groups was significantly lower than the control group, while eNOS activation in DM + LLLT group was higher than the control and LLLT group. ERK activation level in DM + LLLT group also significantly higher than the control group. In AKT phosphorylation and VEGF level, no statistical difference was found among groups.
Conclusions: The present results showed LLLT has a positive effect on PAD mice with DM, including increasing blood perfusion and preventing muscle atrophy
List of Contents
CHAPTER 1 INTRODUCTION 1
CHAPTER 2 LITERATURE REVIEW 2
2.2 Peripheral artery disease 3
2.3 Muscle atrophy in DM and PAD 4
2.4 Low-level laser therapy 5
2.4.1 Low-level laser therapy in enhance revascularization 5
2.4.2 Low-level laser therapy in muscle regeneration 6
2.5 Angiogenesis in PAD 6
2.5.1 Role of VEGF in angiogenesis. 7
2.5.2 Role of Nitric Oxide (NO) production and eNOS 7
2.5.3 ERK 1/2 (Extracellular signal-regulated kinases 1/2) 8
2.6 Muscle regeneration, protein synthesis 8
CHAPTER 3 MATERIAL and METHODS 9
3.1 Animal 9
3.2 Study Drug, and Laser source 9
3.3 Lower extremity artery disease with a diabetic mice model 9
3.3.1 STZ-induced diabetic mice model 9
3.3.2 Peripheral artery disease model 10
3.4 LLLT treatment 10
3.5. Euthanized and sample collect 10
3.5 Western blot 11
3.6. ELISA 11
3.7 Immunofluorescence staining 12
3.8 Statistical analysis 13
CHAPTER 4 RESULTS 14
4.1 Effect of LLLT on blood perfusion on PAD mice with DM 14
4.2 Effect of LLLT on muscle mass 14
4.2.1 LLLT sustain muscle mass after femoral artery ligation 14
4.2.2. LLLT retain muscle fiber sizes after femoral artery ligation 14
CHAPTER 5: DISCUSSION 16
CHAPTER 6: CONCLUSION 20
References 21
Figure 27

List of Figures



Figure 27
Figure 1 27
Figure 2 28
Figure 3 29
Figure 4 30
Figure 5 31
Figure 6 32
Figure 7 33
Figure 8 34
Figure 9 36
Figure 10 38
Figure 11 40
Figure 12 42
Figure 13 44
References
1.International Diabetes Federation. 2019.
2.Clark, N., Peripheral Arterial Disease in People With Diabetes. Diabetes Care, 2003: p. 3333-3341.
3.Jude, E.B., et al., Peripheral arterial disease in diabetic and nondiabetic patients: a comparison of severity and outcome. Diabetes Care, 2001. 24(8): p. 1433-7.
4.Cury, V., et al., Low level laser therapy increases angiogenesis in a model of ischemic skin flap in rats mediated by VEGF, HIF-1alpha and MMP-2. J Photochem Photobiol B, 2013. 125: p. 164-70.
5.Dawood, M.S., A.R. Al-Salihi, and A.W. Qasim, Laser therapy of muscle injuries. Lasers Med Sci, 2013. 28(3): p. 735-42.
6.ADA, Standards of Medical Care in Diabetes. 2019.
7.Atkinson, M.A., G.S. Eisenbarth, and A.W. Michels, Type 1 diabetes. Lancet, 2014. 383(9911): p. 69-82.
8.Hirsch, A.T., et al., Peripheral arterial disease detection, awareness, and treatment in primary care. JAMA, 2001. 286(11): p. 1317-24.
9.Rafieian-Kopaei, M., et al., Atherosclerosis: process, indicators, risk factors and new hopes. Int J Prev Med, 2014. 5(8): p. 927-46.
10.Shu, J. and G. Santulli, Update on peripheral artery disease: Epidemiology and evidence-based facts. Atherosclerosis, 2018. 275: p. 379-381.
11.Lawall, H., et al., The Diagnosis and Treatment of Peripheral Arterial Vascular Disease. Dtsch Arztebl Int, 2016. 113(43): p. 729-736.
12.Hammes, H.P., Pathophysiological mechanisms of diabetic angiopathy. J Diabetes Complications, 2003. 17(2 Suppl): p. 16-9.
13.McDermott, M.M., et al., Lower extremity ischemia, calf skeletal muscle characteristics, and functional impairment in peripheral arterial disease. J Am Geriatr Soc, 2007. 55(3): p. 400-6.
14.Perry, R.A., Jr., et al., The Akt/mTOR pathway: Data comparing young and aged mice with leucine supplementation at the onset of skeletal muscle regeneration. Data Brief, 2016. 8: p. 1426-32.
15.Lin, F., et al., Lasers, stem cells, and COPD. J Transl Med, 2010. 8: p. 16.
16.Posten, W., et al., Low-level laser therapy for wound healing: mechanism and efficacy. Dermatol Surg, 2005. 31(3): p. 334-40.
17.Cotler, H.B., et al., The Use of Low Level Laser Therapy (LLLT) For Musculoskeletal Pain. MOJ Orthop Rheumatol, 2015. 2(5).
18.Farivar, S., T. Malekshahabi, and R. Shiari, Biological effects of low level laser therapy. J Lasers Med Sci, 2014. 5(2): p. 58-62.
19.Moore, P., et al., Effect of wavelength on low-intensity laser irradiation-stimulated cell proliferation in vitro. Lasers Surg Med, 2005. 36(1): p. 8-12.
20.Szymanska, J., et al., Phototherapy with low-level laser influences the proliferation of endothelial cells and vascular endothelial growth factor and transforming growth factor-beta secretion. J Physiol Pharmacol, 2013. 64(3): p. 387-91.
21.Chu, Y.H., et al., Low-level laser therapy prevents endothelial cells from TNF-alpha/cycloheximide-induced apoptosis. Lasers Med Sci, 2018. 33(2): p. 279-286.
22.de Medeiros, M.L., et al., Effect of low-level laser therapy on angiogenesis and matrix metalloproteinase-2 immunoexpression in wound repair. Lasers Med Sci, 2017. 32(1): p. 35-43.
23.Chargé, S.B. and M.A. Rudnicki, Cellular and molecular regulation of muscle regeneration. Physiol Rev, 2004. 84(1): p. 209-38.
24.Shefer, G., et al., Low-energy laser irradiation promotes the survival and cell cycle entry of skeletal muscle satellite cells. J Cell Sci, 2002. 115(Pt 7): p. 1461-9.
25.Weiss, N. and U. Oron, Enhancement of muscle regeneration in the rat gastrocnemius muscle by low energy laser irradiation. Anat Embryol (Berl), 1992. 186(5): p. 497-503.
26.Rodrigues, N.C., et al., Low-level laser therapy (LLLT) (660nm) alters gene expression during muscle healing in rats. J Photochem Photobiol B, 2013. 120: p. 29-35.
27.de Souza, T.O., et al., Phototherapy with low-level laser affects the remodeling of types I and III collagen in skeletal muscle repair. Lasers Med Sci, 2011. 26(6): p. 803-14.
28.Dhalla N.S., C.R.O., Elimban V., Dhadial R.S., Xu YJ, Role of Skeletal Muscle Angiogenesis in Peripheral Artery Disease. Advances in Biochemistry in Health and Disease,, 2017. 6: p. 517–532.
29.Karamysheva, A.F., Mechanisms of angiogenesis. Biochemistry (Mosc), 2008. 73(7): p. 751-62.
30.Aiello, L.P. and J.S. Wong, Role of vascular endothelial growth factor in diabetic vascular complications. Kidney Int Suppl, 2000. 77: p. S113-9.
31.Chen, C.A., et al., Phosphorylation of endothelial nitric-oxide synthase regulates superoxide generation from the enzyme. J Biol Chem, 2008. 283(40): p. 27038-47.
32.Kimura, H. and H. Esumi, Reciprocal regulation between nitric oxide and vascular endothelial growth factor in angiogenesis. Acta Biochim Pol, 2003. 50(1): p. 49-59.
33.Nagareddy, P.R., et al., Increased expression of iNOS is associated with endothelial dysfunction and impaired pressor responsiveness in streptozotocin-induced diabetes. Am J Physiol Heart Circ Physiol, 2005. 289(5): p. H2144-52.
34.Berra, E., et al., Signaling angiogenesis via p42/p44 MAP kinase and hypoxia. Biochem Pharmacol, 2000. 60(8): p. 1171-8.
35.Jones, N., et al., ERK1/2 is required for myoblast proliferation but is dispensable for muscle gne expression and cell fusion. Journal of Cellular Physiology, 2001. 186: p. 104-115.
36.Egerman, M.A. and D.J. Glass, Signaling pathways controlling skeletal muscle mass. Crit Rev Biochem Mol Biol, 2014. 49(1): p. 59-68.
37.Karar, J. and A. Maity, PI3K/AKT/mTOR Pathway in Angiogenesis. Frontiers in molecular neuroscience, 2011. 4: p. 51-51.
38.Furman, B.L., Streptozotocin-Induced Diabetic Models in Mice and Rats. Curr Protoc Pharmacol, 2015. 70: p. 5 47 1-5 47 20.
39.Niiyama, H., et al., Murine model of hindlimb ischemia. J Vis Exp, 2009(23).
40.Wu, K.K. and Y. Huan, Streptozotocin-induced diabetic models in mice and rats. Curr Protoc Pharmacol, 2008. Chapter 5: p. Unit 5 47.
41.Shen, C.C., Y.C. Yang, and B.S. Liu, Large-area irradiated low-level laser effect in a biodegradable nerve guide conduit on neural regeneration of peripheral nerve injury in rats. Injury, 2011. 42(8): p. 803-13.
42.Lopez, A. and C. Brundage, Wound Photobiomodulation Treatment Outcomes in Animal Models. J Vet Med, 2019. 2019: p. 6320515.
43.Mohiuddin, M., et al., Critical Limb Ischemia Induces Remodeling of Skeletal Muscle Motor Unit, Myonuclear-, and Mitochondrial-Domains. Sci Rep, 2019. 9(1): p. 9551.
44.Saied, G.M., et al., The diabetic foot and leg: combined He-Ne and infrared low-intensity lasers improve skin blood perfusion and prevent potential complications. A prospective study on 30 Egyptian patients. Lasers Med Sci, 2011. 26(5): p. 627-32.
45.Chen, C.H., H.S. Hung, and S.H. Hsu, Low-energy laser irradiation increases endothelial cell proliferation, migration, and eNOS gene expression possibly via PI3K signal pathway. Lasers Surg Med, 2008. 40(1): p. 46-54.
46.Li, Y., et al., Low-level laser therapy induces human umbilical vascular endothelial cell proliferation, migration and tube formation through activating the PI3K/Akt signaling pathway. Microvasc Res, 2020. 129: p. 103959.
47.Tian, J., et al., Inhibition of iNOS protects endothelial-dependent vasodilation in aged rats. Acta Pharmacol Sin, 2010. 31(10): p. 1324-8.
48.Miyabara, E.H., et al., Mammalian target of rapamycin complex 1 is involved in differentiation of regenerating myofibers in vivo. Muscle & nerve, 2010. 42(5): p. 778-787.
49.Zhang, L., et al., Low-power laser irradiation promotes cell proliferation by activating PI3K/Akt pathway. 2009. 219(3): p. 553-562.
50.Rhee, Y.-H., Moon, J.-H., Choi, S.-H., & Ahn, J.-C, Low-Level Laser Therapy Promoted Aggressive Proliferation and Angiogenesis Through Decreasing of Transforming Growth Factor-β1 and Increasing of Akt/Hypoxia Inducible Factor-1α in Anaplastic Thyroid Cancer. Photomedicine and Laser Surgery, 2016. 34(6): p. 229-235.
51.Pellicioli, A.C., et al., Laser phototherapy accelerates oral keratinocyte migration through the modulation of the mammalian target of rapamycin signaling pathway. J Biomed Opt, 2014. 19(2): p. 028002.
52.Shingyochi, Y., et al., A Low-Level Carbon Dioxide Laser Promotes Fibroblast Proliferation and Migration through Activation of Akt, ERK, and JNK. PLOS ONE, 2017. 12(1): p. e0168937.
53.Ceolotto, G., et al., Hyperglycemia Acutely Increases Monocyte Extracellular Signal-Regulated Kinase Activity in Vivo in Humans. The Journal of Clinical Endocrinology & Metabolism, 2001. 86(3): p. 1301-1305.
54.Steiler, T.L., et al., Effect of hyperglycemia on signal transduction in skeletal muscle from diabetic Goto-Kakizaki rats. Endocrinology, 2003. 144(12): p. 5259-67.
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top
無相關期刊