蜂胶对紫杉醇处理大鼠的免疫调节和抗毒素作用

S. Fathy, Noha I Said
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引用次数: 5

摘要

本研究旨在探讨蜂胶对紫杉醇(PTX)治疗大鼠的潜在免疫调节和抗毒素作用。本研究选用24只雄性Sprague Dawley大鼠,随机/平均分为4组;对照组,PTX组腹腔注射PTX 5 mg/kg(1次/周),蜂胶组口服蜂胶50 mg/kg /d,最后一组同时注射PTX和蜂胶。所有治疗疗程均为四周。结果显示,与对照组相比,PTX组脾核因子κ B (Nf-κb)基因表达明显上调。此外,与对照组相比,PTX组脾脏肿瘤坏死因子-α、干扰素-γ、C-X-C基序配体10、CC基序配体2和白细胞介素(IL)-4浓度显著升高,IL-10浓度显著降低。此外,与对照组相比,PTX导致骨髓细胞中微核多染红细胞的频率显著升高。另一方面,与对照组相比,单独使用蜂胶处理对所有这些参数没有显著影响。然而,蜂胶显著降低了ptx治疗大鼠所有记录的副作用。综上所述,蜂胶可作为PTX的佐剂,通过下调脾脏Nf-κb基因的表达,减少骨髓微核的形成,调节脾脏免疫细胞的细胞因子和趋化因子的释放,抵消PTX对骨髓细胞的遗传毒性作用
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IMMUNOMODULATION AND ANTIGENOTOXIC EFFECTS OF PROPOLIS IN PACLITAXEL-TREATED RATS
The current study aimed to investigate the potential immunomodulatory and antigenotoxic impacts of propolis in paclitaxel (PTX)-treated rats. Twenty four male Sprague Dawley rats were used in the present study and randomly/equally divided into four groups; control group, PTX group that was intraperitoneally injected with 5 mg/kg PTX (once/week), propolis group that received orally/daily 50 mg/kg propolis, and the last group received both PTX and propolis. All treatments were given for four weeks. The results showed a significant upregulation in the nuclear factor kappa B (Nf-κb) gene expression in the spleen of PTX group, as compared with the control group. In addition, substantial increases in tumor necrosis factor-α, interferon-γ, C-X-C motif ligand 10, CC motif ligand 2, and interleukin (IL)-4 concentrations, while a significant reduction in IL-10 concentration, were detected in the spleen of PTX group compared with the control group. Moreover, PTX resulted in a significant elevation in the frequency of micronucleated polychromatic erythrocytes in bone marrow cells compared with the control group. On the other hand, the treatment with propolis alone did not significantly affect all of these parameters, as compared with the control group. However, propolis decreased significantly all recorded side effects in the PTX-treated rats. In conclusion, propolis can be used as an adjunct with PTX to modulate the cytokines and chemokines release of splenic immune cells, as well as to counteract the genotoxic effect of PTX on bone marrow cells, through downregulating the splenic Nf-κb gene expression, and reducing the bone marrow micronuclei formation, respectively
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