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Two new cardenolides, kalantubolide A (1) and kalantubolide B (2), and two bufadienolide glycosides, kalantuboside A (3) and kalantuboside B (4), aswell as eleven known compounds were isolated and characterized from the EtOH extract of Kalanchoe tubiflora. The structures of compounds were assigned based on 1D and 2D NMR spectroscopic analyses including HMQC, HMBC, and NOESY. Biological evaluation indicated that cardenolides (1-2) and bufadienolide glycosides (3-7) showed strong cytotoxicity against four human tumor cell lines (A549, Cal-27, A2058, and HL-60) with IC50 values ranging from 0.01 µM to 10.66 µM. Cardenolides (1-2) also displayed significant cytotoxicity toward HL-60 tumor cell line. In addition, compounds 3, 4, 5, 6, and 7 blocked the cell cycle in the G2/M-phase and induced apoptosis in HL-60 cells. [ABSTRACT FROM AUTHOR]

Considering the prevalence of cardiovascular disease in public health and the limited validated therapeutic options, this study aimed to find novel compounds targeting the angiotensin II type 1 receptor, accepted as a therapeutic target in cardiovascular disease. A small library consisting of 89 compounds from 39 Chinese herbs was profiled using a cell-based calcium mobilization assay which was developed and characterized for high-throughput screening. [6]-Gingerol derived from Zingiber officinale Roscoe (ginger) was identified as a novel angiotensin II type 1 receptor antagonist, with an IC50 value of 8.173 μM. The hit was further tested by a specificity assay indicating that it had no antagonistic effects on other evaluated GPCRs, such as endothelin receptors. The major ingredient of ginger, [6]-gingerol, could inhibit angiotensin II type 1 receptor activation, which partially clarified the mechanism of ginger regulating blood pressure and strengthening heart in the cardiovascular system. [ABSTRACT FROM AUTHOR]

The purpose of this research is to investigate the effect of tanshinone IIA, an extract of the Chinese medicine Que Xie Hua Yu Tang, on uric acid nephropathy (UAN) and to elucidate the underlying mechanisms. UAN rat model was established. Fifty UAN rats were randomly allocated into 5 groups: adenine-treated group, allopurinol-treated group, and low/middle/high dose of tanshinone IIA-treated groups. Meanwhile, another 10 rats were used as normal controls. Serum uric acid (UA), blood urea nitrogen (BUN), serum creatinine (Scr), MCP-1, and IL-1β levels were measured. Histological staining was performed. Comparison between the adenine group and treatment (allopurinol and tanshinone IIA) groups showed compound treatment could attenuate the inflammation status of the kidneys and decrease serum UA levels. Among different kinds of medicine, tanshinone IIA had similar effects as allopurinol and exerted anti-inflammatory and renal protective effect in a dose-dependent manner. Furthermore, we found tanshinone IIA alone could also inhibit urate-induced MCP-1 and IL-1β overexpression both in vivo and in vitro, accompanied with inhibition of NF-κB translocation from cytosome to nucleus. Tanshinone IIA could protect rats from uric acid-induced kidney damage, probably by attenuating renal inflammatory status. [ABSTRACT FROM AUTHOR]