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1.
Article in Chinese | WPRIM | ID: wpr-906419

ABSTRACT

Objective:To study the effect of Gegen Qinliantang (GQT) on the structure of intestinal flora in dysbacterial diarrhea rats by 16S rRNA sequencing. Method:Sixty healthy SD rats were randomly and equally divided into a control group, a model group, high-, medium-, and low-dose GQT groups, and a Bifidobiogen group. The rat model was induced in the five groups except the control group by administration of mixed antibiotics (178.6 mg·kg<sup>-1</sup> cefradine and 31.25 mg·kg<sup>-1 </sup>gentamicin sulfate) according to the dose. Drug intervention was carried out in each group (7.02, 3.51, and 1.755 g·kg<sup>-1</sup> GQT for the high-, medium-, and low-dose GQT groups, 0.125 g·kg<sup>-1</sup> bifidobacterium capsules for the Bifidobiogen group, and sterile distilled water for the control and model groups) with a volume of 10 mL·kg<sup>-1</sup> for seven days. Colon contents of rats were obtained under anesthesia. The extracted fecal DNA underwent 16S rRNA high-throughput sequencing and the results were analyzed. Result:GQT was proved capable of adjusting the species number and Alpha and Beta diversity, improving the biological richness and diversity of the flora, and positively regulating three differential phyla (Firmicutes, Proteobacteria, and Bacteroidetes) and 14 differential genera (<italic>Bacteroides</italic>,<italic> Parabacteroides</italic>,<italic> Blautia</italic>, etc.) in rat model of dysbacterial diarrhea. Conclusion:The present study confirmed the regulatory effect of GQT on intestinal flora of dysbacterial diarrhea rats, and revealed the physiological and pathological mechanism between intestinal flora and dysbacterial diarrhea.

2.
Article in Chinese | WPRIM | ID: wpr-906261

ABSTRACT

Diabetes has become one of the fastest growing public health issues in the world. Its pathological mechanism is complex and affected by multiple factors. There are trillions of microbes in the human intestine, which are roughly divided into three types: probiotics, neutral bacteria, and pathogenic bacteria. They are in a dynamic balance and constitute a complex intestinal micro-ecosystem. The balance and homeostasis of the intestinal micro-ecosystem are essential to maintain the stability of the body's environment and human health. With the rapid development of high-throughput sequencing technology, imbalanced intestinal flora distribution has been proven to be an important factor in promoting the development of insulin resistance (IR), thus increasing the risk of diabetes. In recent years, the regulation of intestinal flora has become a new approach and new target for the prevention and treatment of diabetes and its complications. The application of traditional Chinese medicine (TCM) in treatment of metabolic diseases such as diabetes and obesity has a long history. TCM has its unique characteristics and advantages, however, the unclear mechanism of action has limited its modernization and industrialization. The harmonious symbiosis between the intestinal flora and the host is consistent with the TCM theory of "harmony between human and nature". The effect of TCM on the intestinal microflora has gradually become a hot topic in medical research today. One study believes that diabetes originates from "intestinal fever". At present, some relevant experimental researches and clinical research literatures have shown that some heat-clearing Chinese herbal compounds have a certain regulating effect on imbalanced intestinal flora. Therefore, the relationship between intestinal flora and diabetes was explored, and the mechanism of heat-clearing Chinese herbal compounds (Da Chaihutang, Gegen Qinliantang, Huanglian Jiedutang, and Wumeiwan) in preventing and treating heat syndrome of diabetes through regulation of intestinal flora was analyzed, in order to provide new theoretical basis and research clues for the further development of drugs for treating diabetes.

3.
Article in Chinese | WPRIM | ID: wpr-906138

ABSTRACT

Objective:Considering the efficacy of Gegen Qinliantang (GQT) in releasing exterior and clearing interior to alleviate dampness-heat dysentery, we analyzed the mechanism of the chloroform extract of GQT in alleviating enterotoxicity caused by irinotecan to provide an experimental basis for the development of GQT. Method:Kunming mice (<italic>n</italic>=60) were randomly divided into a blank group, a model group, a loperamide group (positive drug of loperamide hydrochloride capsule, 0.4 mg·kg<sup>-1</sup>), and high- (2.3 g·kg<sup>-1</sup>) and low-dose (1.16 g·kg<sup>-1</sup>) GQT chloroform extract groups. The mouse model of delayed diarrhea was established by intraperitoneal injection of irinotecan hydrochloride (CPT-11, 55 mg·kg<sup>-1</sup>) for four consecutive days, meanwhile, the mice in the blank group only received the same volume of normal saline. Corresponding drugs were administered by gavage on the fifth day, respectively, while the ones in the blank group and model group were given distilled water for five consecutive days. The general condition of mice in each group was observed, and diarrhea indexes of mice were recorded. Pathological changes in colon tissues of mice were observed by hematoxylin-eosin (HE) staining. The tumor necrosis factor (TNF)-<italic>α</italic>, interleukin (IL)-1<italic>β</italic>, cyclooxygenase (COX)-2, intercellular adhesion molecule (ICAM)-1, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO) levels in colon tissues were detected with the assay kits. Furthermore, the expression levels of Kelch sample epoxy chloropropane associated protein 1 (Keap1), nuclear factor E<sub>2</sub> related factor 2 (Nrf2), tight junction protein-1 (ZO-1), heme oxygenase-1 (HO-1) and tight junction protein (Occludin) were detected by Western blot. Result:Compared with the blank group, the model group showed declined body weight and reduced contents of GSH-Px and SOD (<italic>P</italic><0.01), whereas increased diarrhea indexes and TNF-<italic>α</italic>, IL-1<italic>β</italic>, COX-2, ICAM-1, MDA and NO levels (<italic>P</italic><0.01). Abundant inflammatory cells and colonic mucosa with defects, swelling, bleeding, and inflammatory exudation were revealed by HE staining in the mice of the model group. The expression levels of Keap1, Nrf2, ZO-1, HO-1 and Occludin in colon tissues significantly declined (<italic>P</italic><0.01). Compared with the model group, the loperamide group and the high- and low-dose GQT chloroform extract groups exhibited improved weight loss, reduced diarrhea indexes, diminished TNF-<italic>α</italic>,<italic> </italic>IL-1<italic>β</italic>, COX-2, ICAM-1, MDA and NO, and elevated GSH-Px and SOD. HE staining indicated that the cells were compactly arranged with clear nuclei in the high- and low-dose GQT chloroform extract groups, and the expression levels of Keap1, Nrf2, HO-1, Occludin, and ZO-1 were up-regulated. Conclusion:GQT chloroform extract may alleviate CPT-11-induced delayed diarrhea by regulating inflammation and oxidative stress for enhancing the intestinal barrier function. These findings are expected to provide a reference for exploring the toxicity-attenuating effect of Chinese medicinals on chemotherapy drugs and for developing famous classical formulas.

4.
Article in Chinese | WPRIM | ID: wpr-906005

ABSTRACT

Gegen Qinliantang, a classic traditional Chinese medicine(TCM) compound, has been verified in modern research to possess various pharmacological effects such as anti-inflammation,anti-oxidative stress,protecting intestinal mucosal barrier, and regulating intestinal flora and immune response. Ulcerative colitis (UC) is a chronic idiopathic inflammatory disease involving the colorectal mucosa, which mainly results from genetic susceptibility, intestinal mucosal barrier damage, abnormal immune response, intestinal flora disturbance, and bile acid metabolism disorders. By reviewing the literature published in recent years, this paper sorted out the relevant pathways and mechanisms involved in the treatment of UC by Gegen Qinliantang to provide ideas for further clinical and basic research. This literature review uncovered that Gegen Qinliantang exerted the therapeutic effects against UC mainly via interleukin-6(IL-6)/Janus tyrosine kinase 2(JAK2)/signal transducer and activator of transcription 3(STAT3) signaling pathway, Toll like receptor 4(TLR4)/nuclear transcription factor-κB(NF-κB) signaling pathway,Notch signaling pathway, and matrix metalloproteinase-9(MMP-9)/p38 mitogen-activated protein kinase(p38 MAPK) signaling pathway. Gegen Qinliantang regulates the intercellular molecular transmission in multiple pathways to protect the intestinal mucosal barrier, adjust the immune response and anti-oxidative stress, and relieve UC, demonstrating the multi-target, multi-mechanism, and multi-pathway advantages of TCM compounds.

5.
Article in Chinese | WPRIM | ID: wpr-905826

ABSTRACT

Objective:To explore the protective effect of Gegen Qinliantang on the intestinal mucosal epithelial barrier function of ulcerative colitis (UC) mice, and to explore its mechanism of action in the treatment of ulcerative colitis via matrix metallopeptidase-9 (MMP-9)/p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. Method:The 48 female C57BL/6 mice were randomly divided into normal group, model group, sulfasalazine group (0.3 g·kg<sup>-1</sup>) and Gegen Qinliantang high, medium and low dose groups (2.84,1.42,0.71 g·kg<sup>-1</sup>). The UC murine model was established by 3% dextran sulfate sodium (DSS). Gegen Qinliantang and sulfasalazine were intragastrically administered on the 8<sup>th</sup> day after the model was established for 7 days, and the normal group was treated with the same amount of normal saline. Colon tissues were collected after the last administration, and the pathological changes of colon tissues were detected by hematoxylin-eosin (HE) staining. The expression of tight junction (TJ) proteins such as Occludin and zonula occludens-1(ZO-1) in colon tissues was detected by immunohistochemistry (IHC), and the expression levels of tumor necrosis factor-alpha (TNF-<italic>α</italic>), interleukin-1<italic>β</italic> (IL-1<italic>β</italic>), and MMP-9 mRNA in colon tissues were detected by Real-time polymerase chain reaction (Real-time PCR). The expression of phosphorylated p38 MAPK (p-p38 MAPK), p38 MAPK and MMP-9 protein in colon tissues was detected by Western blot. Result:Compared with normal group, the body weight of mice decreased (<italic>P</italic><0.01) and disease activity index (DAI) score increased significantly (<italic>P</italic><0.01) in model group, the colon tissues of the model group were damaged more obviously, the expression of occludin and ZO-1 proteins in model group was significantly reduced (<italic>P</italic><0.01), and the relative expression levels of TNF-<italic>α</italic>, IL-1<italic>β</italic>, and MMP-9 mRNA in model group were significantly increased (<italic>P</italic><0.01), the expression of p-p38 MAPK and MMP-9 in model group was significantly increased (<italic>P</italic><0.01). Compared with model group, the body mass and DAI score of the sulfasalazine group and Gegen Qinliantang group were significantly improved (<italic>P</italic><0.05,<italic>P</italic><0.01), the colonic tissues damage were significantly improved, and the expression of Occludin and ZO-1 protein was significantly increased (<italic>P</italic><0.05,<italic>P</italic><0.01), the relative expression levels of TNF-<italic>α</italic>, IL-1<italic>β</italic>, and MMP-9 mRNA were significantly decreased (<italic>P</italic><0.01), and the expression of p-p38 MAPK and MMP-9 was significantly decreased (<italic>P</italic><0.01). The changes in the middle dose group were the most obvious among the various dose groups of Gegen Qinliantang. Conclusion:Gegen Qinliantang repairs the intestinal mucosal barrier function by inhibiting the expressions of MMP-9 and inflammatory cytokines such as TNF-<italic>α</italic> and IL-1<italic>β</italic>, blocking the activation of the p38 MAPK signaling pathway, and increasing the expressions of tight junction protein.

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