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AIM:To observe the effect of Pingwei capsule on the precancerous lesions of gastric cancer(PLGC)cell model induced by N-methyl-N'-nitro-N-nitrosoguanidine(MNNG),and to preliminarily explore its mecha-nism.METHODS:Blank serum and Pingwei capsule-containing serum were prepared for later use.A PLGC cell model was established by MNNG-induced human gastric mucosal epithelial cell line GES-1.To evaluate the model,cell morpho-logical changes were observed under inverted microscope,and the expression of proliferating cell-related antigen Ki67 was detected by immunofluorescence staining.CCK-8 assay was used to screen the optimal intervention concentration and time of serum containing drugs.Reactive oxygen species(ROS)content in cells was detected using a fluorescent probe DCFH-DA.Malondialdehyde(MDA)content was detected by ELISA,and the activity of superoxide dismutase(SOD)and gluta-thione peroxidase(GSH-Px)was detected using biochemical reagents.A novel fluorescent probe JC-10 was used to detect mitochondrial membrane potential.The mRNA expression levels of Ki67 and melanoma differentiation-associated gene-7(MDA-7)were detected by real-time fluorescence quantitative PCR.The protein expression levels of Ki67,interleukin-6(IL-6)and MDA-7 were detected by Western blot.RESULTS:Compared with normal group,the ROS and MDA levels in model group and blank serum group were significantly increased(P<0.01),while the activity of SOD and GSH-Px was significantly decreased(P<0.01).The mitochondrial membrane potential was significantly decreased(P<0.01).The protein expression levels of Ki67 and IL-6 were significantly increased(P<0.01),while the protein expression level of MDA-7 was significantly decreased(P<0.01).There were no significant differences of the above indicators between model group and blank serum group(P>0.05).Compared with blank serum group,the Pingwei capsule-containing serum group showed significantly decreased ROS and MDA levels(P<0.01),significantly increased activity of SOD and GSH-Px(P<0.05),significantly increased mitochondrial membrane potential(P<0.01),significantly decreased protein expres-sion levels of Ki67 and IL-6(P<0.01),and significantly increased protein and mRNA expression levels of MDA-7(P<0.01).CONCLUSION:Pingwei capsule can significantly alleviate MNNG-induced oxidative damage and inflammatory response,and regulate the expression of oncogenes and tumor suppressor genes,thereby playing a role in prevention and treatment of PLGC.
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The angiogenic microenvironment is a new blood vessel with different molecular and functional characteristics that sprouts on the original blood vessels through different mechanisms,which directly affects the process of tumor cell growth,proliferation,and migration and has an important impact on the occurrence and development of precancerous lesions of gastric cancer.Correa mode has shown that precancerous lesions of gastric cancer is the key pathological stage before the occurrence of gastric cancer,and it is of great significance to advance the prevention and treatment strategy to this stage.TCM believes that qi deficiency and blood stasis is the key pathogenesis of precancerous lesions of gastric cancer,and its basic treatment is to replenish qi and remove blood stasis,and based on the syndrome differentiation,drugs with the efficacy of nourishing yin and tonifying stomach,soothing the liver and regulating qi,resolving phlegm and dispersing lumps,and clearing heat and dampness for treatment.This article discussed the correlation between precancerous lesions of gastric cancer and angiogenic microenvironment and its regulatory pathways,and summarized the methods and mechanisms of TCM in the treatment of precancerous lesions of gastric cancer from the perspective of regulating angiogenic microenvironment-related pathways,in order to provide a reference for the treatment of precancerous lesions of gastric cancer with TCM.
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ObjectiveThis study aims to investigate the mechanism in which Celastrus orbiculatus extract （COE） affects the proliferation and differentiation of gastric organoids and the expression of Lgr5 and thus reverses the precancerous lesions of gastric cancer （PLGC） by regulating the leucine-rich repeat containing G protein-coupled receptor 5 （Lgr5）/Wingless （Wnt）/β-catenin signaling pathway based on a gastric organoid injury model. MethodGastric organoids were established based on stem cells of the mouse gastric gland. Gastric organoid injury models were constructed by treating gastric organoids with N-methyl-N'-nitro-N-nitrosoguanidine （MNNG， 0.02 mg·L-1）. Gastric organoid injury models were randomly divided into normal group， model group （0.02 mg·L-1 MNNG）， low， medium， and high dose （5， 10， 20 mg·L-1） groups of COE， and Wnt inhibitor Dickkopf-related protein 1 （DKK1） （0.5 mg·L-1） group， and they were treated with respective agents for 24 h. The number and volume of gastric organoids under different drug concentrations were observed under a microscope. The viability of the gastric organoid injury models was detected by Methyl thiazolyl tetrazolium （MTT） assay. The morphology and pathology of gastric organoids were observed using Hematoxylin and Eosin （HE） staining. The expression levels of Lgr5， Mucin2 （MUC2）， Mucin5AC （MUC5AC）， Mucin6 （MUC6）， Wnt， and β-catenin in gastric organoids under different drug concentrations were detected by Western blot （WB）. ResultCompared with the normal group， the number， volume， and activity of gastric organoids in the model group were decreased （P<0.01）， while the expressions of Lgr5， MUC2， Wnt， and β-catenin were significantly increased （P<0.01）. The expressions of MUC5AC and MUC6 were significantly decreased （P<0.01）. Compared with the model group， the number and volume of gastric organoids in the low， medium， and high dose groups of COE were all improved （P<0.01）， and the vitality of gastric organoids was significantly enhanced （P<0.01）. The effect was the most significant at a COE concentration of 20 mg·L-1 （P<0.01）. The expressions of Lgr5 and MUC2 in the medium and high dose groups of COE were significantly reduced （P<0.01）， while the expression of MUC5AC and MUC6 were significantly increased in the low， medium， and high dose groups of COE （P<0.05， P<0.01）. Compared with the model group， Wnt inhibitors could promote the expression of MUC5AC and MUC6 in gastric organoids （P<0.05， P<0.01） and reduce the expression of MUC2， Wnt， and β-catenin. In addition， the combined use of COE at high concentrations and Wnt inhibitors could further promote this trend （P<0.01）. ConclusionCOE inhibits the Wnt/β-catenin pathway by inhibiting the expression of Lgr5， MUC2， Wnt， and β-catenin and promoting the expression of MUC5AC and MUC6， thus promoting the proliferation and differentiation of gastric organoids and reversing the PLGC process.
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Objective To investigate the therapeutic effect and mechanism of Jianwei Xiaozhang Tablets on rats with precancerous lesions of gastric cancer(PLGC).Methods Forty male SD rats were randomly divided into the normal group,the model group,the folic acid group and the Jianwei Xiaozhang Tablets group,with 10 rats in each group.In addition to the normal group,the other three groups of rats were prepared by gavage with Ranitidine Aqueous Solution combined with N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)solution drinking method for the preparation of PLGC model.After successful modeling,drugs were administered accordingly for 7 weeks.The changes in body mass of rats during modeling and drug administration were recorded,the gross view of the stomach was observed and scored pathologically,the coefficients of spleen and liver were determined,the pathological changes in gastric tissue were observed by hematoxylin-eosin(HE)staining,enzyme-linked immunosorbent assay(ELISA)was used to measure serum gastrin(GAS),motilin(MTL)and glucagon(GC),Alisin Blue-Periodic Acid Schiff's(AB-PAS)staining was used to observe the thickness of the mucosal layer of gastric tissues,the expressions of phosphatidylinositol 3-kinase(PI3K),phosphorylated PI3K(p-PI3K),protein kinase B(Akt),phosphorylated Akt(p-Akt),and endothelial-type nitric oxide synthase(eNOS)proteins in gastric tissues were detected by protein immunoblotting(Western Blot),and the expression of vascular endothelial growth factor A(VEGFA)protein in gastric tissues was detected by immunofluorescence staining.Results Compared with the normal group,the body mass of rats in the model group grew slowly during the experimental period,gastric macroscopic pathological scores were significantly increased(P＜0.01),splenic coefficient and hepatic coefficient were significantly decreased(P＜0.01),the gastric tissues showed cuprocyte hyperplasia and intestinal chemotaxis,gastric tissues'inflammation scores were significantly increased(P＜0.01),the serum GAS content was significantly increased(P＜0.01),and the MTL,GC contents were significantly reduced(P＜0.05),and the thickness of the mucous membrane layer of gastric tissue was significantly reduced(P＜0.05),the protein expression levels of PI3K,p-PI3K,Akt,p-Akt and eNOS were reduced(P＜0.01),and the protein expression level of VEGFA was reduced(P＜0.01);compared with the model group,the above indexes of the Jianwei Xiaozhang Tablets group and the folic acid group were all significantly improved(P＜0.05 or P＜0.01),among which,the Jianwei Xiaozhang Tablets group had a better improvement effect in the proliferation of cup cells and intestinal chemotaxis in gastric tissues,the content of serum GAS,and the thickness of the mucous layer in gastric tissues.Conclusion The mechanism of the improvement of PLGC in rats by Jianwei Xiaozhang Tablets may be related to the activation of the PI3K-Akt-eNOS pathway,which in turn promotes the angiogenesis and repair of gastric damaged tissues.
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ObjectiveTo investigate the effect of Qi-invigorating and blood-activating therapy on the miR216b/Beclin1 pathway in mice with atrophic precancerous lesions of gastric cancer （PLGC） and analyze its mechanism in autophagy of PLGC. MethodSeventy-five healthy male SPF KM mice were randomly divided into a blank group and a model group. Mice in the model group were given 1-methyl-3-nitroso-1-nitrosoguanidine （MNNG） solution （150 mg·L-1） for free drinking and gavage and ranitidine solution （0.03 g·kg-1） daily for 12 weeks. According to the random control table， mice were divided into a model group， a Qi-invigorating group （3.5 g·kg-1 of Astragali Radix）， a blood-activating group （0.7 g·kg-1 of Notoginseng Radix et Rhizoma powder）， a Qi-invigorating and blood-activating group （3.5 g·kg-1 of Astragali Radix + 0.7 g·kg-1 of Notoginseng Radix et Rhizoma powder）， and a folic acid group （2 mg·kg-1）. The corresponding drugs were given to mice in each group for 8 weeks and then the tissues were collected. Hematoxylin-eosin （HE） staining was carried out to observe the changes in gastric mucosa. Western blot was used to detect the protein expression of microtuble-associated protein 1 light chain 3 （LC3）Ⅰ， LC3Ⅱ， and Beclin1. Real-time polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of Beclin1 and miR-216b. ResultPathological observation showed that as compared with the blank group， the intrinsic glands of gastric mucosa decreased with atrophy and intestinal metaplasia in the model group， which were improved in all treatment groups， and the improvement of the Qi-invigorating and blood-activating group was the most obvious. As compared with the blank group， the content of LC3Ⅰ， LC3Ⅱ， LC3Ⅱ/LC3Ⅰ， and Beclin1 protein in gastric tissues of the model group was significantly decreased （P<0.05）. As compared with the model group， the content of LC3Ⅰ， LC3Ⅱ， LC3Ⅱ/LC3Ⅰ， and Beclin1 protein in gastric tissues of each treatment group was increased （P<0.05， P<0.01）. The increase was most obvious in the Qi-invigorating and blood-activating group. As compared with the blank group， the mRNA expression of Beclin1 in the model group was decreased （P<0.05）， and that of miR216b was increased （P<0.05）. As compared with the model group， the mRNA expression of Beclin1 was increased and that of miR216b was decreased in each treatment group （P<0.05）， and the changes were the most obvious in the Qi-invigorating and blood-activating group. ConclusionThe mechanism of the Qi-invigorating and blood-activating therapy， represented by Astragali Radix and Notoginseng Radix et Rhizoma， in treating PLGC may be through inhibiting the expression of miR216b and activating Beclin1， thus promoting autophagy and repairing gastric mucosa.
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Gastric cancer is one of the most common malignant tumors of the digestive system， with a high incidence， a low overall survival rate， and poor prognosis after treatment. It has become a major public health problem that threatens the lives and health of people. Since the pathogenesis of gastric cancer is still not fully unraveled， it is difficult to implement primary prevention. Therefore， the research on secondary prevention of gastric cancer， i.e.， precancerous lesions of gastric cancer， is extremely important and has become the focus of many researchers. Precancerous lesions of gastric cancer are the key pathological links in the transformation of inflammatory lesions of gastric mucosa into gastric cancer， including chronic atrophic gastritis， intestinal metaplasia， and dysplasia. Relevant studies have confirmed that with the aggravation of gastric mucosal lesions， the incidence and risk of gastric cancer also increase. Therefore， early diagnosis and effective intervention in the pathological link of gastric precancerous lesions is a key measure to prevent and reduce the incidence of gastric cancer， with great significance. More studies have shown that traditional Chinese medicine （TCM） can truncate and reverse the pathological grading of gastric mucosa， and can also effectively improve the clinical symptoms and quality of life of patients， with few adverse reactions and low recurrence rate， which has unique advantages and characteristics. The theory of ''pathogen invading nutrient and blood aspects'' was first proposed by WU Youxing， a febrile disease doctor， in Treatise on Pestilence （《温疫论》）. It was originally used for the treatment of syndrome changes in the late stage of febrile epidemics， but after being enriched and developed by different doctors， it is now mostly used to guide the treatment of various chronic diseases. Precancerous lesions of gastric cancer are a common and difficult disease in clinical practice. Its evolution process is characterized by asthenia in origin and sthenia in superficiality and deficiency-excess in complexity， which is consistent with the core pathogenesis of ''pathogen invading nutrient and blood aspects''， namely， positive deficiency and intruding pathogen， and intruding pathogen cementation in the blood vessels. They are also interlinked in terms of treatment principles. Therefore， with the theory of ''pathogen invading nutrient and blood aspects'' as the breakthrough point， this article expounded the intervention effect of TCM on precancerous lesions of gastric cancer from the perspective of this theory， reflecting its important guidance and application value and providing new ideas for clinical treatment of diseases.
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Precancerous lesions of gastric cancer (PLGC) is a pathological change accompanied by intestinal metaplasia and dysplasia on the basis of chronic atrophic gastritis. It is also an important stage of "inflammation-cancer transformation" on gastric mucosa. Paying attention to the intervention of PLGC has important value and significance for the secondary prevention of gastric cancer. PLGC has the characteristics of occult onset, toxin damaging collaterals, and long course of disease, which is highly consistent to the pathogenesis characteristics of incubative pathogenic factors. Based on the relevance of incubative pathogenic factors and PLGC, treatment of PLGC from the perspective of incubative pathogenic factors should be mainly strengthening the spleen and stomach, and combined with the methods of regulating qi and dissipating dampness, and removing blood stasis and detoxification. It should also pay attention to the prognosis.Paying attention to the body-mind treatment can reduce the re-occurrence , so as to provide a new way of thinking for treating PLGC from incubative pathogenic factors.
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Objective:To evaluate the value of serum pepsinogen Ⅰ and Ⅱ combined with gastrin-17 in screening precancerous lesions of gastric cancer in physical examination population.Methods:Serum pepsinogen, gastrin-17 and Helicobacter pylori (Hp) antibody were detected in 18 354 physical examination people from July to December 2017 in Wenrong Hospital, Hengdian, Dongyang. The patients were divided into youth group (18 to 39 years old), middle-aged group (40 to 59 years old) and elderly group (≥60 years old) according to their ages. The correlation between the serological level of the above indexes and age was analyzed; according to the new ABC method, the test results were divided into groups A, B, C and D. The patients in group C and D were examined by gastroscopy. The differences of gastric mucosal atrophy or intestinal metaplasia and other precancerous lesions detected by gastroscopy in different age groups were compared.Results:Finally, 18 354 cases were enrolled, including 9 614 males and 8 740 females. With the increase of age, the proportion of group C and D increased gradually. In group C, 181 cases underwent gastroscopy, including 39 cases of atrophic gastritis, 29 cases of intestinal metaplasia and 3 cases of dysplasia/intraepithelial neoplasia, the detection rate of precancerous lesions was 39.23%; in group D, 94 cases underwent gastroscopy, including 22 cases of atrophic gastritis and 13 cases of intestinal metaplasia, the detection rate of precancerous lesions was 37.23%. The proportion of gastric precancerous lesions in group C and D was 29.63% in the young group, 69.70% in the middle-aged group and 71.58% in the old group, respectively. There was significant difference compared with the young group ( P<0.01); atypical hyperplasia occurred in 2.02% and 9.47% of the middle-aged group and the elderly group. Conclusions:The combined detection of serum pepsinogen Ⅰ and Ⅱ and gastrin-17 levels is of great value in the screening of precancerous lesions of gastric cancer; when this method used for early gastric cancer screening in healthy population, it is necessary to consider the influence of age for the risk stratification of gastric cancer.
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Traditional Chinese Medicine (TCM) has certain advantages in the treatment of precancerous lesions of gastric cancer (PLGC) based on the holistic concept and the thought of syndrome differentiation. Currently, it is generally divided into 6 kinds of syndromes: liver and stomach qi stagnation syndrome, liver and stomach heat stagnation syndrome, spleen and stomach weakness syndrome (including spleen and stomach qi deficiency syndrome with coldness), spleen and stomach damp heat syndrome, stomach yin deficiency syndrome and blood stasis in stomach collateral syndrome. Clinically, the doctor should treat PLGC patients according to different syndrome types by using Chinese medicine prescription, which could improve the gastric mucosal pathological state, gastroscopy and clinical symptoms, to rehibit the development of precancerous lesions, reduce the incidence rate of gastric cancer. In the future, the doctors shouldreach the consensus of treating PLGC with TCM diagnosis, and focus on the research of TCM compounds or monomers with obvious curative effect, increase the times of follow-up, and evaluate the long-term curative effect.
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At present， the incidence and mortality of gastric cancer in China are 10.26% and 12.45%， ranking the second and third places， respectively， in the incidence and mortality of malignant tumors in China. Cancer often goes through three stages： precancerous lesions， carcinoma in situ， and invasive carcinoma. It is of great significance to advance cancer prevention and control to the stage of precancerous lesions. The popularization of digestive endoscopy-assisted diagnosis and treatment has enabled the timely diagnosis and treatment of early gastric cancer and severe dysplasia. However， the endoscopic mucosal resection is not suitable for most precancerous lesions of gastric cancer （PLGC）， and the effective drugs are not available. The long-term clinical dynamic monitoring has imposed considerable physical and mental burdens on patients. Gastrointestinal microenvironment is a dynamic balance system composed of gastrointestinal flora， chemical barrier， mechanical barrier， immune barrier， and gastrointestinal nerves. The imbalance of gastric microenvironment has been proved to be the key mechanism of PLGC. According to traditional Chinese medicine （TCM）， PLGC is a result of long-term interaction between deficient healthy Qi and excessive pathogens. In syndrome differentiation and treatment， PLGC is often believed to be developed from chronic gastritis. Besides， the inflammation-cancer transformation model put forward by Correa and the evolution of its TCM pathogenesis are also considered. Guided by the basic treatment principle of reinforcing healthy Qi to eliminate pathogenic factors， we determined the basic therapeutic methods as follows： invigorating spleen， clearing heat， and resolving dampness. At the same time， such methods as soothing liver and regulating Qi， resolving phlegm and dissipating mass， activating blood and resolving stasis， clearing heat and removing toxin， and tonifying deficiency can be combined based on the results of syndrome differentiation. After discussing the correlation between the imbalance of gastric microenvironment and PLGC and summarizing TCM intervention methods and mechanisms against PLGC from the perspective of gastric microenvironment regulation， this paper believed that TCM improved the gastric microenvironment by regulating the disorder of gastric flora， eliminating the gastric mucosal inflammation， and relieving the abnormal immune response， thereby preventing and controlling the PLGC.
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Objective To establish a rat chronic atrophic gastritis with dysplasia model and observe the effect of Shidan granules on the positive expression of NF-κB p65 in gastric tissues and the extent of IKKβprotein content in gastric tissues of chronic atrophic gastritis with dysplasia model rats. Methods Seventy SPF male Wistar rats were randomly divided into the blank group and 60 into the model group. In addition to the blank group, the modeling group was made using the MNNG-based comprehensive modeling method (150 μg/ml MNNG 5 ml/kg each stomach, containing 0.03％ ranitidine feed, free drinking 0.1％ ammonia), and then model successed at the 28th week. The remaining rats in the modeling group were randomly divided into 5 groups: the model group with intragastric administration of gavage, the western medicine group with intragastric administration of viralin, the Shidan granules group with intragastric administration of low/medium/high concentration Chinese medicine decoction. After 12 weeks of treatment, they were sacrificed and the expression of NF-κB p65 and IKKβ was measured and compared. Results Compared with the model group, the average optical density of NF-κBp65 (0.387 ± 0.011, 0.252 ± 0.022, 0.193 ± 0.003 vs. 0.442 ± 0.035) and the expression level of IKKβ (0.309 ± 0.056, 0.216 ± 0.025, 0.125 ± 0.016 vs. 0.405 ± 0.042) in the low-, middle- and high-dose Shidan granules groups significantly decreased (all Ps<0.01). Conclusions The mechanism of improving the precancerous lesions of gastric cancer by Shidan granules may be achieved by inhibiting the expression of IKK, reducing the abnormal activation of NF-κB.
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Gastric cancer is a disease with high morbidity and mortality in the world, and also obtains attention in the global medicine. The occurrence of gastric cancer is a multi-stage and multi-factor process. A large number of epidemiological, pathological and clinical evidences have confirmed that the risk of gastric cancer in patients with chronic atrophic gastritis (CAG) is significantly correlated with the mortality of gastric cancer. Gastric mucosal atrophy, intestinal metaplasia (especially incomplete colonic metaplasia) and dysplasia are the main stages of precancerous lesions of precancerous lesions of gastric cancer (PLGC). Monitoring the condition of CAG patients, especially those with intestinal metaplasia and dysplasia, is of great significance for the discovery of early gastric cancer. CAG and PLGC are great significance in the pathological stage of gastric carcinogenesis. In recent years, more and more in-depth clinical and experimental studies have been carried out in this direction. So far, animal experiment is the main research way for CAG and PLGC disease, so it is very important to explore the modeling method. Choosing a stable and reliable model is the primary factor to study animal experiment. In view of the relationship between two diseases, this paper will summarize the methods of establishing animal models for CAG and PLGC in recent years, generally including chemical drug mutagenesis, physical stimulation, immune modeling, Helicobacter pylori infection replication and surgical modeling. Examples would be given for the application of various methods in the previous experiments, and the author would make a brief comment on the merits and demerits of these methods, which have been explored and successfully made by the author. This study would provide certain reference for the establishment and application of animal models in further CAG and PLGC experiments.
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Objective To discuss the clinical efficacy of compound gastritis mixture (CGM) in treating precancerous lesions of gastric carcinoma (PLGC).Methods Totally 85 PLGC patients were randomly divided into treatment group and control group. The treatment group took CGM and the control group took Vitacoenzyme tablets. One therapeutic course was three months, and the treatment lasted for two courses. The clinical symptoms, electronic gastroscopy presentation, and pathological tissues before and after treatment were observed, the clinical efficacy was evaluated.Results There was statistical significance in TCM syndrome between the two groups (P<0.05), and the effective rate in the treatment group was more obvious than that in the control group (P<0.01). The symptoms of the two groups were significantly improved (P<0.05,P<0.01), but the improvements of the main symptoms in the treatment group were superior to those in the control group (P<0.05,P<0.01). The total effective rate of electronic gastroscopy presentation was 80.0% (36/45) in the treatment group, which was better than that of the control group (P<0.05). Pathological curative effects of chronic atrophic gastritis, intestinal metaplasia, and dysplasia in the treatment group were also better than those in the control group (P<0.05).Conclusion CGM has definite clinical efficacy in treating PLGC.
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This study was aimed to observe the therapeutic effect and mechanism ofQi-Zhu Er-Zhu Er-Cao Tang(QZEZECT) in the treatment of chronic atrophic gastritis (CAG) precancerous lesion. A total of 56 clean grade healthy Wistar rats were randomly divided into 6 groups. In the negative control group (NC), model group,Wei-Fu-Chun(WFC) group,Ren-Zhu Jian-Wei Ke-Li(RZJWKL, RZ) group, there were 10 rats in each group. In the high-dose QZEZECT (QZ-H) group and low-dose QZEZECT (QZ-L) group, there were 8 rats in each group. CAG/PLGC model was established by MNNG in the model group, WFC group, RZ group, QZ-H group and QZ-L group. Intragastric administration of corresponding decoctions at the dose of 0.39 g·kg-1, 3.2 g·kg-1, 54.4 g·kg-1, 13.6 g·kg-1 were given to rats in the WFC, RZ, QZ-H and QZ-L groups once a day for 28 consecutive days, respectively. The same volume of normal saline was given to the NC group and the model group. Histomorphological changes of gastric mucous membrane in rats of each group were observed. Expressions of NF-κB/p65 and CyclinE protein were detected. The results showed that compared with the NC group, the degrees of infiltration and dysplasia and expressions of NF-κB/p65 and CyclinE significantly increased in the model group with statistical significance (P < 0.01). Compared with the model group, the expression of NF-κB/p65 and CyclinE in the WFC group reduced with statistical significance (P < 0.05). The expression of NF-κB/p65 and CyclinE in the RZ and QZ-L group obviously reduced with statistical significance (P < 0.01). The overall effective rates of WFC group, RZ group, QZ-H group and QZ-L group were 50%, 63.3%, 43.3% and 73.3%, respectively. It was concluded that QZEZECT can treat CAG precancerous lesion, which may take effect by improving and inhibiting pathologic changes of the transcription factor of inflammation.
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Objective To observe the effects of Weipixiao on the ultrastructure of gastric mucosa capillaries in rats with precancerous lesions of gastric cancer ( PLGC). Methods The rats were randomized into six groups, including normal group, model group, Vatacoenayme Tablets group ( 0.2 g·kg-1·d-1) , and high-, middle-, and low- dose Weipixiao groups ( 15, 7.5, and 3.75 g·kg-1·d-1 respectively) . The rats received spontaneous intake of N-methyl-N’-nitro-nitrosoguanidine ( MNNG, 200 μg/mL) solution combined with irregular diet and intragastric administration of purgative herbs Xiao Chengqi Decoction ( 2 mL, containing 1 g/mL crude drug) for 18 weeks to induce spleen-deficiency PLGC. The pathological changes in gastric mucosa and the ultrastructure of gastric mucosa capillaries were observed under the transmission electron microscope. Results The model has been established successfully. Transmission electron microscopy results in the model group showed as severely swollen endothelial cells of gastric mucosa capillaries, severely-narrowing or even blocked vascular lumens, rough and discontinuous basement membrane, and swollen, degenerated or even absent pericytes. And the ultrastructure of gastric mucosa capillaries in high-, middle-, and low- dose Weipixiao groups were improved to some degrees, the effect of low-dose Weipixiao group being the best. Conclusion The improvement of the mucosal microcirculation of spleen-deficiency PLGC rats may be one of the pathohistological mechanisms of Weipixiao for spleen-deficiency PLGC.
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Objective: To observe the curative effect of Yiwei Huayu Powder (YHP) and the expression of Th1/Th2 cytokines in patients with precancerous lesions of gastric cancer (PLGC). Methods: There were 100 diagnosed chronic atrophic gastritis (CAG) with gastric mucous membrane dysplasia (Dys) and/or intestinal metaplasia (IM) patients who were randomly divided into treatment group (50 cases) and control group (50 cases). The patients in the treatment group were administrated with YHP for three months, while the other one with Teprenone Capsules and folic acid. Results: Compared with the control group, the symptom scores of the patients in the treatment group decreased more obviously (P < 0.05). Compared with the control group, the pathological scores of the patients in the treatment group decreased more obviously (P < 0.05). After the treatment, the expression of the Th1 (IL-2, INF-γ) level escalated and the Th2 (IL-4, IL-6) level decreased in the treatment group, which existed an obvious difference compared to the control group (P < 0.05). Conclusion: YHP has played a therapeutic effect in patients with PLGC through intervening immune drift and inducing tumor cell apoptosis, thereby blocking or reversing the development of PLGC.
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0.05). The PCNA and Ki-67 expression of blood stasis syndrome is more evident than of Qi stagnation (P
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Objective To explore the effect of Renzhu Jianwei Granules(Granule of Semen Coicis and Rhizoma Atractylodis Macro- cephalae for strengthening the stomach)on the patients with precancerous lesions of gastric cancer(PLGC)and its mechanism. Methods The 58 patients of chronic atrophic gastritis(CAG)complicated with intestinal metaplasia(IM)and/or dysplasia(Dys) were randomized into treatment group and control group with 29 in each.The treatment group was administered Renzhu Jianwei Gran- ules while the control group was given Weifuchun Tablets.The numbers of positive cells of carcinoembryonic antigen(CEA)and cy- clooxygenase 2(COX-2)of gastric mueosa before and after treatment were observed.Results The scores of positive cells of CEA and COX-2 of gastric mucosa of both groups were greatly reduced after treatment(P0.05).Conclusion Renzhu Jianwei Granules can reduce CEA and COX-2 of PLGC patients,possibly being one of the mechanisms in treating PLGC.