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Mucormycosis is an infectious disease characterized by rapidly progressive vascular invasiveness, thrombosis and tissue necrosis, which could be potentially responsible for blocking the exudation of leukocytes to infection sites and affecting drug distribution. Glucose-regulated protein 78 (GRP78) is a key protein involved in regulating the invasiveness of Mucorales. Endoplasmic reticulum GRP78 is overexpressed under various stress conditions and transported to the cell membrane to become a cell surface receptor for Mucorales entering into vascular endothelial cells. This article reviewed the mechanisms and pathogenesis of GRP78-mediated host cell invasion and summarized the progress in related targeted drugs, aiming to provide reference for developing multi-target intervention against mucormycosis.
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Objective To investigate the chemical preventive effect of matrine on ethyl nitrate nitroguanidine nitrate induced gastric cancer in rats. Methods 100 male Wistar rats were selected and randomly divided into four groups,each had 25 rats ,treated with different drugs respectively.Rats in the negative control group (group A)freely drunk water;each rat in gastric carcer model group (group B)drunk ethyl nitrate nitroguanidine nitrate (ENNG)1.5 mg/d by themselves;gastric cancer model rats of experimental group (group C)drunk matrine 150 mg/(kg · d)ethyl nitrate nitroguanidine nitrate (ENNG)150mg/(kg·d)by themselves;negative control group (group D)rats drunk matrine for injection 150 mg/(kg·d)by themselves.Rats were killed after 24 weeks,rats were observed on gastric mucosa change by naked eye and microscope ,and detected proliferating cell nucleus antigen (PCNA)of stomach tissue ,levels of serum transforming growth factorβ1 (TGF-β1 )and B cell lymphoma/leukemia-2 (Bcl-2).Results Canceration rate [64.00% (16/25)]of the rat gastric mucosa in Group B was significantly higher than that in group C [12.00% (3/25)],and the difference was statistically significant (P<0.05 );PCNA,TGF-β1 and the Bcl-2 level of rats in group C was lower than those in group B,and the difference was statistically significant (P<0.05 );after raising 24 weeks,change rate of gastric mucosa atrophy and hyperplasia in group B were significantly higher than those of group C,and the difference was statistically significant (P<0.05 );after raising 24 weeks,there was no cancerous changes on gastric mucosa in group A and D ,and the change of gastric mucosa atrophy and hyperplasia had no obvious difference,there was no statistically significant difference.Conclusion Matrine could inhibit rat gastric cancer induced by ENNG by lowering PCNA,TGF-β1 and the Bcl-2 levels,which provides evidence for the potential chemical preventive effect on human gastric cancer.
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This study is to investigate therapeutic effect of astaxanthin on acetic acid-induced gastric ulcer in rats. Rats were divided into control group, ulcer control group, and astaxanthin (5, 10, and 25 mg x kg(-1)) groups at random, 8 rats in each group. After administered for 10 days consecutively, all the rats were sacrificed. The area of ulcer and the levels of MDA, SOD, CAT and GSH-Px in gastric mucosa were measured. Compared with ulcer control group, in astaxanthin (5, 10, and 25 mg x kg(-1)) groups, the area of ulcer was decreased significantly. Level of MDA decreased while activities of SOD, CAT and GSH-Px increased (P < 0.05). Astaxanthin has good therapeutic effect on acetic acid-induced gastric ulcer in rats. Eliminating free radical and improving local blood circulation of the ulcer may be the mechanism of action.