Oral glutamine inhibits tumor growth of gastric cancer bearing mice by improving immune function and activating apoptosis pathway
| Autor: | Li-bin Li, Wen-ji Xu, Tai-yong Fang |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Glutamine Administration Oral Apoptosis Biology Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Immune system Stomach Neoplasms In vivo Cell Line Tumor medicine Animals Secretion TUNEL assay Cancer Neoplasms Experimental Cell Biology General Medicine Glutathione medicine.disease Neoplasm Proteins 030104 developmental biology chemistry 030220 oncology & carcinogenesis Cancer research Signal Transduction Developmental Biology |
| Zdroj: | Tissue and Cell. 71:101508 |
| ISSN: | 0040-8166 |
| DOI: | 10.1016/j.tice.2021.101508 |
| Popis: | Gastric cancer is one of the most common cancers in the world. It has been shown that exogenous glutamine (GLN) can inhibit the growth of tumor in vivo, but the relationship between GLN and gastric cancer has not been studied. The gastric cancer bearing mouse model was constructed and taken GLN orally at the same time, and the results found that oral GLN (1 or 2 g/kg/d) significantly inhibited the growth rate of tumor and reduce the weight of tumor tissues. Immunohistochemistry showed that oral GLN significantly reduced the PCNA index, which further proved that GLN could inhibit the growth of tumor cells. At the same time, TUNEL assay showed that oral GLN significantly enhanced the apoptosis levels of tumor cells. In addition, GLN reduced GSH levels in tumor tissues, but increased the levels of GSH in plasma, improved the T-lymphocyte transformation rate and NK cell activity, significantly inhibited the secretion of TNF-α and promoted the secretion of IL-2, thus regulating the immune function in vivo. Further detection of apoptosis pathway showed that oral GLN significantly enhanced the expression of pro-apoptotic factor Bad and inhibited the expression of Bcl-2. Meanwhile, GLN significantly increased the activities of Caspase-3, Caspase-8, caspase-9 and PARP. GSH activator NAC had a similar effect to GLN, which could improve the immune function and activate apoptosis pathway, while GSH inhibitor BSO significantly blocked the regulation of GLN, destroyed the immune balance and inhibited apoptosis, but IL-2 significantly blocked the anti-apoptotic effect of BSO. Therefore, oral GLN can improve immune function and activate apoptosis pathway through GSH, and then inhibit the growth of tumor in vivo. |
| Databáze: | OpenAIRE |
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