ABSTRACT
Objective: To observe the effect of acupoint application therapy of modified Wuzhuyu Binglang Tang on chronic non-atrophic gastritis (CNAG) and the mechanism of action. Method: Two hundred and seventeen patients were randomly divided into control group (107 cases) and observation group (110 cases) by random number table. Both groups' patients got Omeprazole enteric-coated tablets half an hour before meals, 20 mg/time, 2 times/day, bismuth potassium citrate tablets half an hour before meals, 2 tablets/time, 2 times/day, amoxicillin capsules after meals, 1.0 g/time, 2 times/day, two dimensional furazolidone tablets after meals, 1 tablet/time, 2 times/day, mosapride citrate tablets, 5 mg/time, 3 times/day. The treatment lasted for 2 weeks. Patients in observation group got acupoint application of modified Wuzhuyu Binglang Tang at Zhongwan, Weiyu, Geyu, Shenyu and Piyu for 6 h/day, 1 time/day. And the patients in control group got model drug at the same acupoints. Before and after treatment, epigastric fullness and epigastric pain were scored. Levels of motilin, gastrin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and prostaglandin E2 (PGE2) were detected. In 1-month follow-up visit, Hp and adverse reaction were detected under gastroscope. Result: The clinical effect in observation group under gastroscope was better than that in control group (Z=2.015, PZ=2.663, PPχ2=5.002, P2 was higher than that in control group (PConclusion: The acupoint application therapy of modified Wuzhuyu Binglang Tang can relieve the clinical symptoms, promote the negative conversion rate of Hp, improve the clinical effect, regulate gastrointestinal hormones, inhibiting release of inflammatory factors, protect gastric mucosa, and improve gastrointestinal function, with safety in clinic use.
ABSTRACT
<p><b>OBJECTIVE</b>To study the main mechanisms of Aitongxiao Recipe (ATXR) for anti-tumor at the molecular level, and to clarify different efficient drugs' roles in anti-tumor, thus in-depth explaining the objectivity and substance of "cancer toxic" theory.</p><p><b>METHODS</b>Walker-256 tumor strain was used for Wistar rat transplanted liver cancer modeling. After successful modeling rats were randomly divided into 5 groups, i. e., the ATXP group, the qi regulating and blood circulating group (as the assembled I group), the heat clearing and detoxification group (as the assembled II group), the body resistance strengthening and cultivating group (as the assembled III group), and the model group, 10 in each group. Corresponding medication was given to rats in each group for 14 successive days. Finally rats were sacrificed and the tumor mass was taken out. The apoptosis rate and the cell cycle of tumor cells were detected by flow cytometry Annexin V/PI. The protein and mRNA expressions of Bcl-2 and survivin were detected using immunohistochemistry and real-time fluorescent quantitative PCR.</p><p><b>RESULTS</b>(1) The apoptosis of hepatoma carcinoma cells could be obviously promoted in the ATXP group. The cell cycle could also be affected, making major cells arrest at G0/G1 phase. The proliferation of hepatoma carcinoma cells was effectively prevented. The efficacy in the assembled II group was in line with that in the ATXP group with no statistical difference (P>0.05). It was also effective in the assembled III group, but its efficacy was not as good as that in the former two groups, showing statistical difference (P<0.01). (2) ATXP could obviously down-regulate the protein and mRNA expressions of Bcl-2 and survivin in hepatoma carcinoma cells. Drugs for heat clearing and detoxification showed significant effects on down-regulating the protein and mRNA expressions of Bcl-2 and survivin in hepatoma carcinoma cells. Their effects were similar to that of ATXP (P>0.05). The effects of drugs for body resistance strengthening and cultivating were not as good as the former two, showing statistical difference (P<0.01). Drugs for blood circulating and stasis removing could up-regulate the protein and mRNA expressions of Bcl-2 and survivin to some extent.</p><p><b>CONCLUSIONS</b>(1) ATXP could increase the apoptosis ratio of hepatoma carcinoma cells obviously through down-regulating the protein and mRNA expressions of Bcl-2 and survivin, thus inhibiting their proliferation. (2) Drugs for heat clearing and detoxification played the most important roles in ATXP. The evil heat and dampness (damp-heat insidious pathogen) is the most fundamental carcinogenic factors. The insufficiency of vital qi is also one of the pathogenic factors. The mechanisms of phlegm, stasis, and other pathological products are not clear and await further studies.</p>