Koul Ashwani, Garg Shaffy, Mohan Vandana
Department of Biophysics, Basic Medical Science Block II, Panjab University, Chandigarh, India.
Drug Chem Toxicol. 2021 Nov;44(6):642-654. doi: 10.1080/01480545.2019.1643877. Epub 2019 Aug 5.
The aim of the present study is to divulge the chemopreventive potential of arabinogalactan (AG) on benzo(a)pyrene [B(a)P] induced initiation of lung carcinogenesis. AG is one of the naturally occurring bioactive polysaccharides which is widely found in medicinal plants. Male Balb/c mice were divided into four experimental groups. Group I served as control. Group II animals were injected with B(a)P (50 mg/kg b. wt. i.p.). Group III animals were administered with AG (7.5 mg/kg b.wt.) orally. Group IV animals received B(a)P and AG as in group II and group III, respectively. B(a)P treatment in mice resulted in imbalance of carcinogen metabolizing enzymes and respiratory marker enzymes at 2nd, 6th and 10th week of the experimental protocol. Also, it leads to the increased protein synthesis as depicted by increased argyrophilic nucleolar organizer regions (AgNOR) positive cells and altered histopathological features. Studies on bronchoalveolar lavage fluid (balf) of B(a)P exposed animals revealed increase in surface tension when compared with control counterparts. Apart from target tissue (lung), B(a)P also led to the clastogenic damage in other tissues (spleen and bone marrow) as depicted by increase in percentage of micronucleus cells at different time intervals. Treatment with AG efficiently counteracted all the above anomalies and restored cellular homeostasis. These observations suggest that AG has the potential to modulate B(a)P induced changes in the pulmonary tissue as well as other tissues which could have implications in delaying the initiation of carcinogenesis, however, further investigations are required to explore its complete mechanism of action.
本研究的目的是揭示阿拉伯半乳聚糖(AG)对苯并(a)芘[B(a)P]诱导的肺癌发生起始阶段的化学预防潜力。AG是一种天然存在的生物活性多糖,广泛存在于药用植物中。雄性Balb/c小鼠被分为四个实验组。第一组作为对照组。第二组动物腹腔注射B(a)P(50mg/kg体重)。第三组动物口服AG(7.5mg/kg体重)。第四组动物分别如第二组和第三组那样接受B(a)P和AG。在实验方案的第2周、第6周和第10周,小鼠接受B(a)P处理导致致癌物代谢酶和呼吸标记酶失衡。此外,如嗜银核仁组织区(AgNOR)阳性细胞增加所示,它还导致蛋白质合成增加,并改变了组织病理学特征。对暴露于B(a)P的动物的支气管肺泡灌洗液(BALF)的研究显示,与对照动物相比,表面张力增加。除了靶组织(肺)外,B(a)P还导致其他组织(脾和骨髓)的染色体断裂损伤,如不同时间间隔微核细胞百分比增加所示。用AG治疗有效地抵消了上述所有异常,并恢复了细胞稳态。这些观察结果表明,AG有可能调节B(a)P诱导的肺组织以及其他组织的变化,这可能对延迟癌症发生起始阶段有影响,然而,需要进一步研究以探索其完整的作用机制。