食用淡水蜗牛提取物对砷诱导的大鼠组织损伤的治疗潜力是通过抗氧化机制和抑制促炎反应来确定的

Sk. Sajed Ali, S. Maiti
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引用次数: 0

摘要

长期接触砷会导致癌症。一些治疗药物在砷中毒治疗中表现出效力不足/副作用。贝拉米亚蜗牛是一种可食用的蜗牛,长期以来一直被少数民族和非少数民族的农村人民用作治疗几种健康异常/肝脏疾病的传统药物。本实验采用砷中毒大鼠模型,探讨其抗氧化机制和抗炎作用对砷致大鼠组织损伤的保护和治疗作用。本研究中,在砷中毒(0.6 ppm/kg体重/天,持续28天)的大鼠和离体大鼠肝脏切片中(单独用亚砷酸钠或与BBE一起在克雷布-林格缓冲液中处理2小时和4小时),同时测试了本品肉提取物(BBE, 1 g/kg体重/天,持续28天)。在大鼠中,BBE通过增强抗氧化系统,强有力地阻止砷诱导的肠上皮组织和肝组织/DNA的氧化/坏死损伤,这在非蛋白可溶性硫醇(NPSH)、超氧化物歧化酶(SOD)和过氧化氢酶的结果中得到了体现,这在DNA阶梯/彗星测定/组织结构结果中得到了清楚的反映。单独砷可降低过氧化氢酶和SOD活性(H2O2/亚砷酸盐氧化应激为透析浓缩SOD),并降低抗氧化信号分子NPSH和血清一氧化氮(NO)水平。与此同时,砷增加了组织丙二醛,导致dna断裂/肝脏损伤,除NO外,这些都被构成高水平磷/抗坏血酸/游离硫醇的BBE所抑制。此外,砷诱导的促炎细胞因子TNF-α的增加被恢复,终止急性期反应。这项研究首次表明,与印度西孟加拉邦自然水平的水污染相比,某些生物体/动物提取物在受到高砷污染的肝脏和肠道组织中的效率有所提高。我们目前的研究结果可能用于开发一些保护/治疗成分,以对抗这种水生生物的砷毒性。需要进一步研究才能得出更结论性的意见。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Therapeutic Potentials of Edible Freshwater-Snail Bellamya Bengalensis Extract against Arsenic-induced Rat Tissue Damage are Conferred by Antioxidative Mechanism and Attenuation of Pro-Inflammatory Response
Chronic arsenic exposure results in cancer. Some therapeutic agents show inadequate-potency/ side-effects in arsenic-toxicity treatment. The Bellamya bengalensis, an edible snail has long been used by rural people comprised of both ethnic and nonethnic groups as traditional medicine in several health-anomalies/ liver-disorders. In an attempt to investigate the possible protective and therapeutic effect against arsenic induced rat tissue damage are conferred by antioxidative mechanism and attenuation of pro-inflammatory response, the extract of B. bengalensis was tested in arsenic intoxicated rat model. Here, Bellamya bengalensis flesh-extract (BBE, 1 g/kg bw/day for 28days) was tested concomitantly in arsenic-intoxicated (0.6 ppm/kg bw/day for 28days) rat, in in-vitro rat liver slices (in Krebs-ringer buffer for 2 and 4 hours treatment with sodium arsenite alone or with BBE). In the rat, BBE strongly prevented arsenic-induced oxidative/necrotic damages to the intestinal epithelial tissue and liver-tissue/DNA by strengthening the antioxidant-system as shown in Non-protein soluble thiol (NPSH), Superoxide Dismutase(SOD) & catalase results which are clearly reflected in DNA-ladder/comet-assay/histo-architecture results. Arsenic alone decreased catalase and SOD activities in-vivo and in-vitro (H2O2/arsenite redox-stress to dialyzed-concentrated SOD) and also decreased antioxidative signaling molecules i.e. NPSH, serum nitric-oxide (NO) levels. At the same time, arsenic increased the tissue malondialdehyde resulting in DNA-breakage/liver-damage which except NO, were restrained by BBE that constitutes high-level of phosphorus/ascorbate/free-thiols. Moreover, an arsenic-induced increase in pro-inflammatory cytokine TNF-α was restored terminating an acute-phase-reaction. This study, for the first-time, shows the efficiencies of some organism/animal extract in hepatic and intestinal tissue challenged with a high level of arsenic with comparison to the natural level water contamination in West Bengal, India. Our present outcome may be utilized for the development of some protective/therapeutic component against arsenic toxicity from this aquatic organism. Further studies are necessary for more conclusive comments.
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