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Abstract：
This study aims to investigate the effect of red ginseng polysaccharide (RGP) on gastric cancer (GC) development and explore its mechanism.
GC cell lines AGS were treated with varying concentrations of RGP (50, 100, and 200 μg/mL). AGS cells treated with 200 μg/mL RGP were transfected with aquaporin 3 (AQP3) overexpression vector. Cell proliferation, viability, and apoptosis were evaluated by MTT, colony formation assay, and flow cytometry, respectively. Real-time quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression of AQP3. The levels of Fe2+, malondialdehyde, and lactate dehydrogenase were measured using their respective detection kits, and the reactive oxygen species levels was determined by probe 2\',7\'-dichlorodihydrofluorescein diacetate. The expression of ferroptosis-related protein and PI3K/Akt pathway-related protein were assessed by western blot. In vivo experiments in nude mice were performed and the mice were divided into four groups (n = 5/group) which gavage administrated with 150 mg/kg normal saline, and 75, 150, 300 mg/kg RGP, respectively. Their tumor weight and volume were recorded.
RGP treatment effectively inhibited the proliferation and viability of AGS cells in a dosage-dependent manner and induced apoptosis. It induced ferroptosis in AGS cells, as well as inhibiting the expression of PI3K/Akt-related proteins. AQP3 overexpression could reversed the effect of RGP treatment on ferroptosis. Confirmatory in vivo experiments showed that RGP could reduce the growth of implanted tumor, with increased RGP concentration resulting in greater tumor inhibitory effects.
RGP might have therapeutic potential against GC, effectively inhibiting the proliferation and viability of AGS cells.
GC cell lines AGS were treated with varying concentrations of RGP (50, 100, and 200 μg/mL). AGS cells treated with 200 μg/mL RGP were transfected with aquaporin 3 (AQP3) overexpression vector. Cell proliferation, viability, and apoptosis were evaluated by MTT, colony formation assay, and flow cytometry, respectively. Real-time quantitative reverse transcription PCR (qRT-PCR) was used to detect the expression of AQP3. The levels of Fe2+, malondialdehyde, and lactate dehydrogenase were measured using their respective detection kits, and the reactive oxygen species levels was determined by probe 2\',7\'-dichlorodihydrofluorescein diacetate. The expression of ferroptosis-related protein and PI3K/Akt pathway-related protein were assessed by western blot. In vivo experiments in nude mice were performed and the mice were divided into four groups (n = 5/group) which gavage administrated with 150 mg/kg normal saline, and 75, 150, 300 mg/kg RGP, respectively. Their tumor weight and volume were recorded.
RGP treatment effectively inhibited the proliferation and viability of AGS cells in a dosage-dependent manner and induced apoptosis. It induced ferroptosis in AGS cells, as well as inhibiting the expression of PI3K/Akt-related proteins. AQP3 overexpression could reversed the effect of RGP treatment on ferroptosis. Confirmatory in vivo experiments showed that RGP could reduce the growth of implanted tumor, with increased RGP concentration resulting in greater tumor inhibitory effects.
RGP might have therapeutic potential against GC, effectively inhibiting the proliferation and viability of AGS cells.
摘要：
■本研究旨在研究红参多糖（RGP）对胃癌（GC）发展的影响并探讨其机制。
用不同浓度的RGP(50、100和200μg/mL)处理GC细胞系AGS。用水通道蛋白3(AQP3)过表达载体转染用200μg/mLRGP处理的AGS细胞。细胞增殖，生存能力，用MTT法评估细胞凋亡，集落形成试验,和流式细胞术，分别。实时定量逆转录PCR(qRT-PCR)检测AQP3的表达。Fe2+的水平，丙二醛，和乳酸脱氢酶使用各自的检测试剂盒进行测量，活性氧水平由探针2'确定，7'-二氯二氢荧光素二乙酸酯。Westernblot检测铁凋亡相关蛋白和PI3K/Akt通路相关蛋白的表达。在裸鼠中进行体内实验，并将小鼠分为四组（n=5/组），分别用150mg/kg生理盐水进行灌胃，和75、150、300毫克/千克RGP，分别。记录它们的肿瘤重量和体积。
■RGP处理以剂量依赖性方式有效抑制AGS细胞的增殖和活力，并诱导细胞凋亡。它在AGS细胞中诱导铁凋亡，以及抑制PI3K/Akt相关蛋白的表达。AQP3过表达可以逆转RGP处理对铁凋亡的影响。证实的体内实验表明，RGP可以减少植入肿瘤的生长，增加RGP浓度导致更大的肿瘤抑制作用。
■RGP可能具有针对GC的治疗潜力，能有效抑制AGS细胞的增殖和活力。
用不同浓度的RGP(50、100和200μg/mL)处理GC细胞系AGS。用水通道蛋白3(AQP3)过表达载体转染用200μg/mLRGP处理的AGS细胞。细胞增殖，生存能力，用MTT法评估细胞凋亡，集落形成试验,和流式细胞术，分别。实时定量逆转录PCR(qRT-PCR)检测AQP3的表达。Fe2+的水平，丙二醛，和乳酸脱氢酶使用各自的检测试剂盒进行测量，活性氧水平由探针2'确定，7'-二氯二氢荧光素二乙酸酯。Westernblot检测铁凋亡相关蛋白和PI3K/Akt通路相关蛋白的表达。在裸鼠中进行体内实验，并将小鼠分为四组（n=5/组），分别用150mg/kg生理盐水进行灌胃，和75、150、300毫克/千克RGP，分别。记录它们的肿瘤重量和体积。
■RGP处理以剂量依赖性方式有效抑制AGS细胞的增殖和活力，并诱导细胞凋亡。它在AGS细胞中诱导铁凋亡，以及抑制PI3K/Akt相关蛋白的表达。AQP3过表达可以逆转RGP处理对铁凋亡的影响。证实的体内实验表明，RGP可以减少植入肿瘤的生长，增加RGP浓度导致更大的肿瘤抑制作用。
■RGP可能具有针对GC的治疗潜力，能有效抑制AGS细胞的增殖和活力。
