ABSTRACT
OBJECTIVE: Gang-Qing-Ning (GQN) is a traditional Chinese medicine formula that has been used in the treatment of hepatocellular carcinoma (HCC) in the folk population for decades. However, scientific validation is still necessary to lend credibility to the traditional use of GQN against HCC. This study investigates the antitumor effect of GQN on H22 tumor-bearing mice and its possible mechanism. METHODS: Fifty H22 tumor-bearing mice were randomly assigned to five groups. Three groups were treated with high, medium, and low dosages of GQN (27.68, 13.84, and 6.92 g/kg, respectively); the positive control group was treated with cytoxan (CTX) (20 mg/kg) and the model group was treated with normal saline. After 10 days' treatment, the tumor inhibitory rates were calculated. Pathological changes in tumor tissue were observed, and the key proteins and genes of the mitochondrial apoptosis pathway were measured, as well as the mRNA expression levels of VEGF in tumor tissue. RESULTS: The tumor inhibitory rates of high, medium, and low dosages of GQN groups were 47.39%, 38.26%, and 22.17%, respectively. The high dosage of the GQN group significantly increased the protein and mRNA expression levels of Bax, Cyt-C, and cleaved Caspase 3 (or Caspase 3) (P < 0.01) but decreased the expression levels of Bcl-2, VEGF, and microvessel density (MVD) (P < 0.01). CONCLUSIONS: The high dosage of GQN can significantly inhibit the tumor growth in H22 tumor-bearing mice. It exerts the antitumor effect by enhancing proapoptotic factors and inhibiting the antiapoptotic factor of the mitochondrial apoptosis pathway and inhibiting tumor angiogenesis.
ABSTRACT
OBJECTIVE: To find out the mechanism of Tangfukang on the diabetic nephropathy(DN). METHOD: A Model of streptorotocin diabetic rats was used. The expressions of the AGEs, ICAM-1, IV-C and FN were observed in renal cortex of diabetic rats with immunohistochemical method. The level of the IL-1 beta in blood serum was measured by radioimmunoassay method and the level of TNF was determined in blood serum by ELISA method. Aminoguanidine was selected as the control medicine which could inhibit the expression of monenzymatic glycosylation end products of protein. All the results were compared to analyze the effect of Tangfukang on monenzymatic glycosylation of protein and cytokine expression in early diabetic nephropathy rats. RESULTS: Both Tangfukang and aminoguanidine significantly decreased the expression of AGEs, but Tangfukang was greatly superior to aminoguanidine in suppressing the expression of cytokine like ICAM-1, IL-1 beta, TNF-alpha and the ingredients of extracellular matrix like IV-C, FN. CONCLUSION: It may be the partical mechanism of Tangfukang to suppress the monenzymatic glycosylation of protein and to reduce the expression of cytokine in diabetes. The effect of Tangfukang is superior to that of aminoguanidine.
