An experimental study of using Chai Lai Prescription to treat in vitro rabbit models of reflux esophagitis.

BACKGROUND: Chai Lai Prescription is a Chinese herbal compound which is used to sooth the liver, strengthen the spleen and harmonize the stomach for descending adverse Qi. We initiated the study to investigate its mechanism of treating in vitro rabbit reflux esophagitis models. METHODS: Adult male Japanese white rabbits, weighing 1.8-2.2 kg, were divided into five groups of three each, which were: normal control group (Krebs buffer, pH7.4), esophagitis model group (Krebs buffer, pH5.8), esophagitis model proup+low-dose Chinese herbal medicine protection group (0.6 mg × ml(-1)× kg(-1)), esophagitis model group+moderate-dose Chinese herbal medicine protection group (6 mg × ml(-1)× kg(-1)), esophagitis model group+high-dose Chinese herbal medicine protection group (60 mg × ml(-1)×kg(-1)). The RT-PCR method was used to test the influence of Chai Lai Prescription on IL-1 and IL-6 in in vitro rabbit models of esophagitis. We treated the in vitro models with different doses of Chinese herbal medicine. RESULTS: Esophageal mucosa were filled with various liquids. IL-6 and IL-1ß mRNA expression was increased in rabbit esophageal mucosa stimulated with acid. Chinese herbal medicine significantly reduced the levels of IL-6 and IL-1ß mRNA expression in the in vitro cultured rabbit esophageal mucosa. Using Chinese herbal medicine to treat in vitro models of RE, we found that the IL-6 and IL-1ß mRNA expression levels went down, near to or lower than the normal control levels, compared with the group treated with acidified buffer solution. CONCLUSIONS: Chai Lai Prescription lowered the IL-1ß and IL-6 cytokine mRNA levels and protected the esophageal mucosa in the in vitro models of reflux esophagitis, suggesting that the traditional Chinese herbal compound may be able to treat reflux esophagitis by inhibiting the its inflammatory mediators.

MYH rs3219476 and rs3219472 polymorphisms and risk of cholangiocarcinoma.

Cholangiocarcinoma (CCA) is a rare but devastating malignancy. Up to 90% of patients presenting with CCA have no identifiable risk factors. The base excision repair (BER) pathway has a principal role in the repair of mutations caused by oxidized or reduced bases. The MutY homolog (MUTYH, MYH) is one of the key proteins in the BER pathway, but the role of MYH in the tumorigenesis of CCA is largely unknown. In this study, we investigated the influence of MYH rs3219476 and rs3219472 polymorphisms on CCA incidence. MYH genotypes were detected using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. We found that for rs3219472, compared with subjects carrying the MYH G/G genotype, those with the A/A genotype had a 2.816-fold higher risk of CCA [odds ratio (OR)=2.816, 95% confidence interval (CI)=0.992-7.999, P=0.047). For rs3219476, compared with subjects carrying the MYH T/T genotype, those with the T/G genotype had a reduced risk of CCA (OR=0.359, 95% CI=0.17-0.758, P=0.006). Our findings suggest that since significantly increased CCA risk was found in individuals with a homozygous variant genotype for rs3219472, it may be a biomarker for screening individuals at high risk of developing the disease.

[Expression of livin in gastric cancer and effect of silencing of the livin gene on apoptosis in gastric cancer cells].

OBJECTIVE: The aim of this study was to detect the expression of livin in human gastric carcinoma and analyze the relationship between livin expression and cliniopathologic features. To explore the feasibility of small interference RNA (siRNA) in inhibition of livin gene expression and to investigate the apoptosis susceptibility of SGC-7901 cells by siRNA-mediated silencing of the livin gene. METHODS: The expression of livin at mRNA and protein levels were determined by RT-PCR and Western blot assay, respectively. The relationship between livin expression and clinicopathologic features was analyzed. Two siRNAs specifically targeting livin gene were designed and synthesized in vitro, and were transfected into the gastric cancer SGC-7901 cells. The expression of livin mRNA was assayed by RT-PCR. Cell growth state and 50% inhibition concentration (IC50) of 5-Fu and cisplatin on SGC-7901 cells were determined by MTT method. Cell apoptosis was assessed by flow cytometry (FCM). RESULTS: The expressions of livin mRNA and protein were detected in 19 of 40 gastric carcinoma cases (47.5%). No expression of livin was detected in tumor-adjacent tissues and benign gastric lesion. A positive correlation was found between livin expression and poor differentiation as well as lymph node metastases (P < 0.05). The level of livin mRNA was decreased in the SGC-7901 cells transfected by si-livin1 for 48 hours, with inhibition of cell growth. IC50 of si-livin-treated SGC-7901 cells to 5-Fu and cisplatin was decreased (P < 0.05) and the cells were more susceptible to proapoptotic stimuli (5-Fu and cisplatin) than control groups (P < 0.05). CONCLUSION: Livin is overexpressed in gastric carcinoma with a correlation to tumor differentiation and lymph node metastasis, suggesting that it may be as one of molecular prognostic factors for some cases of gastric cancer. SiRNA can inhibit livin expression of SGC-7901 cells and induce cell apoptosis. Livin might serve as a new target for apoptosis-inducing therapy of gastric cancer. Livin;