Main Article Content
Catechins inhibits apoptosis through anti oxidant and anti inflamation pathway. Catechins also increases brain-derived neurotrophic factor (BDNF). There was a few research that explained the role of catechins in traumatic brain injury (TBI). The objective of the study was to evaluate the effect of catechins administration on neurologic severity score (NSS) through apoptosis and neurotropic pathway in traumatic brain injury rat model.
A post test only controlled group design was performed using traumatic brain injury rat (Rattus novergicus) model through weight drop models. It was devided into negative control group, positive control group, TBI+catechins 513 mg/kgBW, TBI+catechins 926 mg/kgBW, TBI+catechins 1113 mg/kgBW. NSS was measured in the first hours, day three, and day seven. The expressions of NFkB, TNFa, Bcl-2, Bax, caspase 3, caspase 8, BDNF, and the numbers of apoptosis cells were evaluated by imunohistochemystry method. One way Anova and Kruskal Wwallis were used to analyse the data.
TNFa, caspase 8, number of apoptosis cells were significantly decreased on the seventh day administration compared to the third day administration (p<0.05). Catechins increased the expression of Bcl-2/Bax and BDNF significantly (p<0.05). Yet, there were no significant differences between expression of caspase 3, NSS, Bcl-2/Bax ratio, and BDNF toward third days administration of catechins compared with seven days administration (p>0.050).
Administration of catechins decreased NSS through inhibiting inflammation and apoptosis, as well as induced the neurotrophic factors in rat brain injury. Catechins may serve as a potential intervention for TBI.
Prins M, Greco T, Alexander D, et al. The pathophysiology of traumatic brain injury at a glance. Dis Model Mech 2013;6:1307–15. doi: 10.1242/dmm.011585.
Hinson HE, Rowell S, Schreiber M. Clinical evidence of inflammation driving secondary brain injury: a systematic review. J Trauma Acute Care Surg 2015;78:184–91. doi: 10.1097/TA. 0000000000000468.
Czabotar PE, Lessene G, Strasser A, et al. Control of apoptosis by the Bcl-2 protein family: implications for physiology and therapy. Nat Rev Mol Cell Biol 2014;15:49–63. doi: 10.1038/nrm3722.
Algattas H, Huang JH. Traumatic brain injury pathophysiology and treatments: early, intermediate, and late phases post-injury. Int J Mol Sci 2013;15:309–41. doi: 10.3390/ijms 15010309.
McAllister TW. Neurobiological consequences of traumatic brain injury. Dialogues Clin Neurosci 2011;13:287–300.
Lin X, Li M, Shang A, et al. Neuroglobin expression in rats after traumatic brain injury. Neural Regen Res 2012;7:1960–6. doi: 10.3969/j.issn.1673-5374.2012.25.006.
Patarroyo S, Vargas V. Apoptosis and activation-induced cell death. New York: Intechopen; 2013.
Zhang B, Wang B, Cao S, et al. Epigallocatechin-3-gallate (EGCG) attenuates traumatic brain injury by inhibition of edema formation and oxidative stress. Korean J Physiol Pharmacol 2015;19:491-7. doi: 10.4196/kjpp.2015.19.6. 491.
Chen A, Xiong LJ, Tong Y, et al. The neuroprotective roles of BDNF in hypoxic ischemic brain injury. Biomed Reports 2013;1:167–76. doi: 10.3892/br.2012.48.
Yashin A, Nemzer B, Yashin Y. Bioavailability of tea components. J Food Res 2012;1:281–90. doi: 10.5539/jfr.v1n2p281.
Lorenz M. Cellular targets for the beneficial actions of tea polyphenols. Am J Clin Nutr 2013;98Suppl 6:S1642–50. doi: 10.3945/ajcn. 113.058230.
Jager AK, Saaby L. Flavonoids and the CNS. Molecules 2011;16:1471–85. doi: 10.3390/molecules16021471.
Vauzour D. Dietary polyphenols as modulators of brain functions: Biological actions and molecular mechanisms underpinning their beneficial effects. Oxid Med Cell Longev 2012. Article ID 914273, 16 pages. http://dx.doi.org/10.1155/2012/914273.
Mohamed RH, Karam RA, Amer MG. Epicatechin attenuates doxorubicin-induced brain toxicity: critical role of TNF-a, iNOS and NFkB. Brain Res Bull 2011;86:22–8. doi: 10.1016/j.brainresbull.2011.07.001.
Katergaris N, Dufficy L, Roach P, et al. Green tea catechins as neuroprotective agents: systematic review of the literature in animal preclinical trials. Adv Food Technol Nutr Sci 2015;1:48–57. doi: 10.17140/AFTNSOJ-1-108.
Khalatbary AR, Ahmadvand H. Anti-inflammatory effect of the epigallocatechin gallate following spinal cord trauma in rat. Iran Biomed J 2011;15:31–7.
Itoh T, Tabuchi M, Mizuguchi N, et al. Neuroprotective effect of (–)-epigallocatechin-3-gallate in rats when administered pre- or post-traumatic brain injury. J Neural Transm 2013;120:767–83. doi: 10.1007/s00702-012-0918-4.
Suzuki M, Tabuchi M, Ikeda M, et al. Protective effects of green tea catechins on cerebral ischemic damage. Med Sci Monit 2004;10:BR 166-74.
Xiong Y, Mahmood A, Chopp M. Animal models of traumatic brain injury. Nat Rev Neurosci 2014;14:128–142. doi: 10.1038/nrn3407.
Albert-Wei Benberger C, Várrallyay C, Raslan F, et al. An experimental protocol for mimicking pathomechanism of traumatic brain injury in mice. Exp Transl Stroke Med 2012;4. doi: 10.1186/2040-7378-4-1.
Riawan W, Alfiantya PF, Adianingsih OR, et al. Analysis of the histopathology, TNF-a of microglia cells expression, NRG-I/ erbB oligodendrocyte, and Ki67/ apoptosis of dentate gyrus rattus norvegicus brain after acute traumatic brain injury. Indones J Cancer Chemoprevention 2015;6:20–9.
Ratnawati R, Ciptati, Satuman. Isolasi EGCG dari teh hijau klon GMB4 Jawa Barat. Laporan Progam Insentif Riset Dasar, RISTEK Kementerian Negara Riset dan Teknologi;2009.
Xu J, Ding K, Wang H, et al. Inhibition of cathepsin S produces neuroprotective effects after traumatic brain injury in mice. Mediators Inflamm 2013. doi: 10.1155/2013/187873.
Wu Q, Xuan W, Ando T, et al. Low laser therapy for traumatic brain injury in mice: effect of different wavelengths. Lasers Surg Med 2012;44: 218–26. doi: 10.1002/lsm.22003.
Olmos G, Llado J. Tumor necrosis factor alpha: a link between neuroinflammation and excitotoxicity. Mediators Inflamm 2014. doi: 10.1155/2014/861231.
Cheng T, Wang W, Li Q, et al. Cerebroprotection of flavanol (-) epicatechin after traumatic brain injury via Nrf2-dependent and independent pathways. Free Radic Biol Med 2016;92:15–28. doi: 10.1016/j.freeradbiomed.2015.12.027.
27. Wang L, Li X, Han Y. Neuroprotection by epigallo catechin gallate against bupivacaine anesthesia induced toxicity involves modulation of PI3/Akt/PTEN signalling in N2a and SH-SY5Y cells. Int J Clin Exp Med 2015;8:15065–75.
Schoch KM, Madathil SK, Saatman KE. Genetic manipulation of cell death and neuroplasticity pathways in traumatic brain injury. Neurotherapeutics 2012;9:323–37. doi: 10.1007/s13311-012-0107-z.