2007TumoriRequires access

Influence of resveratrol on the growth of Lewis lung carcinomas in mice and its underlying mechanism

Juan Zhang

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Abstract

Objective: To explore the influence of resveratrol (Res) on the growth of Lewis lung carcinomas in mice and the corresponding mechanism. Methods:The Lewis lung carcinoma model was established in C57BL mice. Forty C57BL mice were randomly divided into 4 groups (n=10): control group, low-dose Res group (2.5 mg·kg-1·d-1), middle-dose Res group (5 mg·kg-1·d-1) and high-dose Res group (10 mg·kg-1·d-1). Mice were given intragastrically with Res for 20 d. All mice were sacrificed on d 22 after inoculation. The volume and weight of tumors were recorded. Microvessel density (MVD) in tumor tissues was measured by immunohistochemistry. The expression level of vascular endothelial growth factor (VEGF) was examined by immunohistochemistry and RT-PCR. The apoptotic index (AI) was determined by TUNEL assay. Results: The tumor growth was suppressed significantly in Res 5 mg and 10 mg·kg-1·d-1 groups. The weights and volumes of Lewis lung carcinoma in both groups above were markedly decreased compared with control group(P0.01). The inhibitory rates were 39.04% and 49.66%, respectively, which was significantly higher than that in Res 2.5 mg·kg-1·d-1 group (12.33%,P0.01). Mice in Res 5 mg and 10 mg·kg-1·d-1 group had markedly lower levels of VEGF expression and MVD and significantly higher AI compared with control group (P0.01). However, Res 2.5 mg·kg-1·d-1 had no obvious influence on VEGF expression, MVD and AI (P0.05). Conclusion: Res remarkably inhibites the growth of Lewis lung carcinoma in mice by inhibiting expression of VEGF, reducing MVD, and promoting apoptosis.

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Objective: To explore the influence of resveratrol (Res) on the growth of Lewis lung carcinomas in mice and the corresponding mechanism. Methods:The Lewis lung carcinoma model was established in C57BL mice. Forty C57BL mice were randomly divided into 4 groups (n=10): control group, low-dose Res group (2.5 mg·kg-1·d-1), middle-dose Res group (5 mg·kg-1·d-1) and high-dose Res group (10 mg·kg-1·d-1). Mice were given intragastrically with Res for 20 d. All mice were sacrificed on d 22 after inoculation. The volume and weight of tumors were recorded. Microvessel density (MVD) in tumor tissues was measured by immunohistochemistry. The expression level of vascular endothelial growth factor (VEGF) was examined by immunohistochemistry and RT-PCR. The apoptotic index (AI) was determined by TUNEL assay. Results: The tumor growth was suppressed significantly in Res 5 mg and 10 mg·kg-1·d-1 groups. The weights and volumes of Lewis lung carcinoma in both groups above were markedly decreased compared with control group(P0.01). The inhibitory rates were 39.04% and 49.66%, respectively, which was significantly higher than that in Res 2.5 mg·kg-1·d-1 group (12.33%,P0.01). Mice in Res 5 mg and 10 mg·kg-1·d-1 group had markedly lower levels of VEGF expression and MVD and significantly higher AI compared with control group (P0.01). However, Res 2.5 mg·kg-1·d-1 had no obvious influence on VEGF expression, MVD and AI (P0.05). Conclusion: Res remarkably inhibites the growth of Lewis lung carcinoma in mice by inhibiting expression of VEGF, reducing MVD, and promoting apoptosis.

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Available abstract

Objective: To explore the influence of resveratrol (Res) on the growth of Lewis lung carcinomas in mice and the corresponding mechanism. Methods:The Lewis lung carcinoma model was established in C57BL mice. Forty C57BL mice were randomly divided into 4 groups (n=10): control group, low-dose Res group (2.5 mg·kg-1·d-1), middle-dose Res group (5 mg·kg-1·d-1) and high-dose Res group (10 mg·kg-1·d-1). Mice were given intragastrically with Res for 20 d. All mice were sacrificed on d 22 after inoculation. The volume and weight of tumors were recorded. Microvessel density (MVD) in tumor tissues was measured by immunohistochemistry. The expression level of vascular endothelial growth factor (VEGF) was examined by immunohistochemistry and RT-PCR. The apoptotic index (AI) was determined by TUNEL assay. Results: The tumor growth was suppressed significantly in Res 5 mg and 10 mg·kg-1·d-1 groups. The weights and volumes of Lewis lung carcinoma in both groups above were markedly decreased compared with control group(P0.01). The inhibitory rates were 39.04% and 49.66%, respectively, which was significantly higher than that in Res 2.5 mg·kg-1·d-1 group (12.33%,P0.01). Mice in Res 5 mg and 10 mg·kg-1·d-1 group had markedly lower levels of VEGF expression and MVD and significantly higher AI compared with control group (P0.01). However, Res 2.5 mg·kg-1·d-1 had no obvious influence on VEGF expression, MVD and AI (P0.05). Conclusion: Res remarkably inhibites the growth of Lewis lung carcinoma in mice by inhibiting expression of VEGF, reducing MVD, and promoting apoptosis.

Key concepts: Lewis lung carcinoma, Immunohistochemistry, TUNEL assay, Vascular endothelial growth factor, Resveratrol, Apoptosis, Lung, Angiogenesis

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