Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
Add filters








Year range
1.
The Korean Journal of Physiology and Pharmacology ; : 403-411, 2021.
Article in English | WPRIM | ID: wpr-896275

ABSTRACT

This study was designed to evaluate the gastroprotective activity of cirsilineol in hydrochloric acid (HCl)/ethanol-induced gastric ulcer model. Cirsilineol was administered at the doses of 20 and 40 mg/kg in HCl/ethanol-induced rats. The gastroprotective ability was verified by determining the ulcer score, total acidity, hemoglobin, inflammatory cytokines, lipid peroxides, and enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) in gastric tissue and serum biochemical analysis. The results showed a favorable increase in the hemoglobin level, antioxidant enzymes (SOD and CAT), restored electrochemical balance (carbon dioxide & anion gap) while a noticeable decrease in ulcer index, total acidity, lipid peroxides, inflammatory cytokines (interleukin-1 beta [IL-1β], IL-6, and tumor necrosis factor alpha) in rats treated with the cirsilineol. The serum biochemical analysis on liver markers (alkaline phosphatases, alanine aminotransferase, and aspartate aminotransferase), kidney markers (urea, creatinine, albumin, globulin, total protein), and lipid profile (triglyceride, high-density lipoprotein, total cholesterol) were attenuated by cirsilineol treatment in rats. Histopathology showed enhanced gastric protection and preserved the integrity of gastric mucosa upon cirsilineol administration. These results ultimately suggest that cirsilineol has gastroprotective effects that prevent the development of gastric ulcer.

2.
The Korean Journal of Physiology and Pharmacology ; : 403-411, 2021.
Article in English | WPRIM | ID: wpr-903979

ABSTRACT

This study was designed to evaluate the gastroprotective activity of cirsilineol in hydrochloric acid (HCl)/ethanol-induced gastric ulcer model. Cirsilineol was administered at the doses of 20 and 40 mg/kg in HCl/ethanol-induced rats. The gastroprotective ability was verified by determining the ulcer score, total acidity, hemoglobin, inflammatory cytokines, lipid peroxides, and enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT) in gastric tissue and serum biochemical analysis. The results showed a favorable increase in the hemoglobin level, antioxidant enzymes (SOD and CAT), restored electrochemical balance (carbon dioxide & anion gap) while a noticeable decrease in ulcer index, total acidity, lipid peroxides, inflammatory cytokines (interleukin-1 beta [IL-1β], IL-6, and tumor necrosis factor alpha) in rats treated with the cirsilineol. The serum biochemical analysis on liver markers (alkaline phosphatases, alanine aminotransferase, and aspartate aminotransferase), kidney markers (urea, creatinine, albumin, globulin, total protein), and lipid profile (triglyceride, high-density lipoprotein, total cholesterol) were attenuated by cirsilineol treatment in rats. Histopathology showed enhanced gastric protection and preserved the integrity of gastric mucosa upon cirsilineol administration. These results ultimately suggest that cirsilineol has gastroprotective effects that prevent the development of gastric ulcer.

3.
Journal of Zhejiang Chinese Medical University ; (6): 208-210, 2016.
Article in Chinese | WPRIM | ID: wpr-491336

ABSTRACT

Objective] To explore the professor Xie Jingri fromthe theory of liver and spleen in the treatment of chronic atrophic gastritis treatment and medication,in order to further understand the relationship among the liver,spleen and stomach. To broaden the thinking,to improve the clinical curative effect of chronic atrophic gastritis. [Method] With factor liver main spleen transportation as the theoretical basis,from the perspective of the relationship between five zang-organs and six fu-organs,with clinical basis for the case of professor Xie Jingri about the theory of liver and spleen in the treatment of chronic atrophic gastritis is discussed for collection. [Results] Professor Xie Jingri putting forward the theory of liver and spleen in the treatment of chronic atrophic gastritis has profound historical origin,there are documentaries, rules on the use of drugs to people,both focus on the overall,with the evidence-based medicine,and attention to detail,judge of modern,pathogenesis. For chronic atrophic gastritis has opened up a more effective treatment. [Conclusion] Through the elaboration of treatment of chronic atrophic gastritis treatment,medication and typical cases,make the theory of liver and spleen for stomach more clear train of thought,on the theory of liver and spleen theory,improve the efficiency of clinical treatment of chronic atrophic gastritis.

4.
Chinese Journal of Information on Traditional Chinese Medicine ; (12): 55-58, 2015.
Article in Chinese | WPRIM | ID: wpr-465082

ABSTRACT

Objective To investigate the effects of capsaicin on the invasion ability of human large cell carcinoma NCI-H460 and the expressions of E-cadherin and Snail;To discuss the possible mechanisms of anti-non-small cell lung cancer.Methods NCI-H460 cells were cultured in vitro and treated with capsaicin at various concentrations, and no capsacin-treated group was set as control group. Effects of capsaicin on NCI-H460 apoptosis, its invasion ability, and the changes in protein expressions of E-cadherin and Snail were evaluated by Hoechst33342 nuclear staining assay, Transwell chamber invasion assay, and Western blot respectively. Results Compared with the control group, Hoechst33342 nuclear staining assay showed that capsaicin could induce NCI-H460 cell apoptosis (P<0.05);Transwell invasion in vitro results showed that capsaicin could significantly inhibit invasion of penetrating cells (P<0.05);Western blot analysis showed that E-cadherin expression level was significantly elevated and snail expression level significantly decreased (P<0.05).Conclusion Capsaicin can induce NCI-H460 cell apoptosis. Decrease the Snail expression and stimulate E-cadherin expression so as to inhibit the invasion ability of NCI-H460, which may be one of its mechanisms of anti-non-small cell lung cancer.

SELECTION OF CITATIONS
SEARCH DETAIL