Chinese Medicine Leptochloa chinensis Inhibits the Malignant Behaviors of Renal Cell Carcinoma 786-O Cells by Regulating the mTOR Pathway.

BACKGROUND: Renal cell carcinoma (RCC) is a common malignant tumor of the urinary system that seriously threatens human life and health. This study aims to explore the role of the traditional Chinese medicine Leptochloa chinensis in the pathogenesis of RCC. Meanwhile, this study also revealed the molecular biological mechanism of its antitumor activity. METHODS: Human RCC 786-O cells were cultured in the RPMI-1640 medium, which contains different concentrations of Leptochloa chinensis (1,000, 3,000, and 9,000 µg/ml). MTT and flow cytometry assays were used to detect the viability of 786-O cells. Transwell and wound healing assays were used to detect cell metastasis. The protein expression was observed by western blot analysis. RESULTS: Leptochloa can inhibit cell proliferation and induce apoptosis in RCC 786-O cells. In addition, Leptochloa can weaken the migration and invasion of 786-O cells. More importantly, Leptochloa can block the mTOR pathway by inhibiting the protein expression of p-mTOR. Moreover, the high concentration of Leptochloa chinensis has a better inhibitory effect on 786-O cells. CONCLUSION: The traditional Chinese medicine Leptochloa chinensis inhibits the viability and metastasis of 786-O cells by blocking the mTOR pathway.

Potassium supplementation blunts the effects of high salt intake on serum retinol-binding protein 4 levels in healthy individuals.

AIMS/INTRODUCTION: Excessive dietary salt or low potassium intakes are strongly correlated with insulin resistance (IR) and type 2 diabetes mellitus. In epidemiological and experimental studies, increased serum retinol-binding protein 4 (RBP4) contributes to the pathogenesis of type 2 diabetes mellitus. Herein, we hypothesized that RBP4 might be an adipocyte-derived "signal" that plays the crucial role in salt-related insulin resistance or type 2 diabetes mellitus. This study aimed to assess whether salt consumption and potassium supplementation influence serum RBP4 levels in healthy individuals. MATERIALS AND METHODS: A total of 42 participants (aged 25-50 years) in a rural area of Northern China were successively provided normal (3 days at baseline), low-salt (7 days; 3 g/day NaCl) and high-salt (7 days; 18 g/day) diets, and a high-salt diet with potassium additive (7 days; 18 g/day NaCl and 4.5 g/day KCl). Urinary sodium and potassium were measured to ensure compliance to dietary intervention. Then, RBP4 levels were evaluated by enzyme-linked immunosorbent assay. RESULTS: High salt intake significantly raised serum RBP4 levels in healthy participants (17.5 ± 0.68 vs 28.6 ± 1.02 µg/mL). This phenomenon was abrogated by potassium supplementation (28.6 ± 1.02 vs 17.6 ± 0.88 µg/mL). In addition, RBP4 levels presented positive (r = 0.528, P < 0.01) and negative (r = -0.506, P < 0.01) associations with 24-h urinary sodium- and potassium excretion levels. CONCLUSIONS: RBP4 synthesis is motivated by high salt intake and revoked by potassium supplementation. Our pioneer work has contributed to the present understanding of salt-induced insulin resistance or type 2 diabetes mellitus.