Background and purpose:To investigate the induction of apoptosis by epigallocatechin-3-gallate(EGCG) in xenograft nude mice with human gastric cancer cells and its molecular mechanism. Methods:Human gastric cancer cells were planted into nude mice in order to establish the cancer model, the different dosages of EGCG were injected intraperitoneally in the nude mice. After treatment, flow cytometry (FCM) was used to detect the apoptosis of implanted tumor cells. Immunohistochemical staining was used to detect the expression of apoptosis-related genes like Bal-2 and Bax in implanted tumor.Results:EGCG significantly inhibited tumor growth after being injecting intraperitoneally in the nude mice. The apoptotic cells in implanted tumor could be detected by flow cytometry with PI staining. The expressions of Bax、Caspase-3 were upregulated and Bcl-2 expression was downregulated in implanted tumor.Conclusions:EGCG could significantly inhibit tumor growth in xenograft nude mice with human gastric cancer cells through inducing apoptosis. The down-regulation of Bcl-2 expression and up-regulation of Bax expression observed could result in the activation of Caspase-3, the pathway might account for the induction of apoptosis.

Objective To investigate the FECH gene mutation in a Chinese family with erythropoietic protoporphyria, to explore the relationship between gene mutation and clinical manifestations so as to estab-lish a basis for the genetic diagnosis and treatment of erythropoietic protoporphyria. Methods Clinical data on a Chinese family with typical EPP was collected. Peripheral blood was obtained from patients, unaffected individuals in the family and 50 unrelated human controls. Genomic DNA was extracted and PCR was per-formed to amplify the whole coding regions (exons 1 to 11) of FECH gene and their flanking intron sequences followed by direct sequencing to detect possible mutations. Results Based on clinical symptom and por-phyrin levels, a diagnosis of erythropoietic protoporphyria was made in 3 family members. DNA fragments of expected size were amplified by PCR. Gene sequencing revealed a heterozygons mutation (IVS1 + 1G >C) in intron 1 of FECH gene in the proband, his sister and father, but not in unaffected family members or unrelated human controls. Also, an IVS1-23C/T polymorphism associated with low expression alleles was observed in intron 1 of FECH gene of the proband, his sister and mother. Conclusions A novel mutation in the donor splice site of intron 1 of FECH gene is first reported in a Chinese family with EPP; this muta-tion may lead to a deficiency of FECH gene and serve as a molecular basis of development of erythropoietic protoporphyria.