Clinical observation of magnesium aluminum carbonate combined with rabeprazole-based triple therapy in the treatment of helicobacter pylori-positive gastric ulcer associated with hemorrhage.

Objectives: To evaluate the clinical effect of magnesium aluminum carbonate combined with rabeprazole-based triple therapy in the treatment of patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage. Methods: A total of 80 patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage admitted to the Baoding First Central Hospital from January 2019 to December 2020 were selected and randomly divided into two groups, with 40 cases in each group. The control group were given rabeprazole-based triple therapy, while the experimental group were treated with magnesium aluminum carbonate on the basis of the control group. The changes of symptoms and signs such as abdominal pain, abdominal distension, nausea, vomiting and hematochezia were compared between the two groups before and after treatment. Serological changes of the gastric mucosal microenvironment, such as the serum levels of extracellular regulatory protein kinase (ERK), superoxide dismutase (SOD) and epidermal growth factor receptor (EGFR), were compared between the two groups. Moreover, the differences in the results of gastroscopy between the two groups before and after treatment were compared and analyzed. Results: The scores of gastrointestinal symptoms in the experimental group after treatment were significantly improved compared with the control group (p=0.00). The levels of ERK and EGFR in the experimental group were significantly lower than those in the control group (ERK, p=0.01; EGRF, p=0.00), while the level of SOD was significantly increased (p=0.02). After treatment, the total effective rate of ulcer healing in the experimental group was 82.5%, which was significantly better than 60% in the control group (p=0.03). After treatment, moderate to severe gastric mucosal inflammation in the experimental group decreased to 10%, significantly better than that in the control group (decreased to 30%) (p=0.03). Conclusion: Magnesium aluminum carbonate combined with rabeprazole-based triple therapy is preferred for the treatment of patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage. With such a highly effective treatment regimen, the internal environment and blood supply of gastric mucosal cells can be significantly improved, gastric mucosal inflammation and gastrointestinal symptoms can be ameliorated, and the healing of ulcer surfaces can be accelerated.

[Inhibitory effects of 17beta-estradiol on spontaneous and activated contraction of rat uterus smooth muscle].

OBJECTIVE: To observe and compare the effects of 17beta-estradiol (EST) on the phasic and tonic contractile activities of the uterine smooth muscles of SD rats in vitro. METHODS: Different concentrations of 17beta-estradiol were added into the perfusion muscular sockets containing uterine smooth muscles of SD rats, and the activities of muscle contraction were recorded at the same time. RESULTS: 17beta-estradiol had obvious depression effects on spontaneous rhythmic contraction of the uterine smooth muscles in a concentration-dependent manner, it could considerably decrease muscular tension, the mean amplitudes and frequencies of contractile waves (P < 0.01); it could also suppress the uterine contraction stimulated by KCl, CaCl2 or prostaglandin F2alpha (PGF2alpha). Based on the contraction of uterine smooth muscle stimulated by KCl, IC50 was 7.278 micromol/L and pD2 was -0.862 when calculated by linear regression method. 17beta-estradiol could also inhibit the maximal CaC12 contraction of uterine smooth muscle in the Ca2+ free Krebs solution, which the ECQ was 1.422 x 10(-3) mol/L, pD2 was 2.847 (control), but the E50 was 3.028 x 10(-3) mol/L, p2 was 2.519 (added with EST) when calculated by linear regression method. CONCLUSION: The depression effects of 17beta-estradiol on the spontaneous rhythmic contraction and activated contraction of the uterine smooth muscles of SD rats could be mediated through the blockage of C2+ influx through potential-dependent Ca2+ channels of plasma membrane.

Effects of estrogen and phytoestrogens on endometrial leakage in ovariectomized rats and the related mechanisms.

Phytoestrogens, a group of plant-derived non-steroidal compounds that can behave as estrogens by binding to estrogen receptors, have drawn great attention for their potentially beneficial effects on human health. However, there are few studies investigating the potential side effects of phytoestrogens on the reproductive system. The present study was to elucidate the effects of 17ß-estradiol (E2), progesterone (P4), and phytoestrogens genistein (Gen), resveratrol (Res), and phloretin (Phl) on eosinophilic infiltration of the ovariectomized rat uterus and endometrial vascular permeability, and to analyze the underlying mechanisms. The ovariectomized rats received daily subcutaneous injections of E2, E2+P4, P4, Gen, Res, Phl, or an equivalent volume of vehicle for 21 days, and sham-operated animals (Sham rats) were used as the controls. Hematoxylin-eosin staining revealed a marked increase in uterine eosinophilic infiltrations in ovariectomized rats treated with E2, E2+P4 or P4, which was associated with increased expression of vascular endothelial growth factor (VEGF), nuclear factor-κB (NF-κB), and tumor necrosis factor-α (TNF-α) proteins as determined by immunohistochemical and Western blot analysis. However, all three phytoestrogens had no markedly effect on the uterine eosinophilic infiltration and the expressions of VEGF, NF-κB, and TNF-α in the uterus of ovariectomized rats. Our data demonstrate that E2 alone or in combination with P4 increases uterine eosinophilic infiltration which is related with vascular hyperpermeability caused by VEGF, NF-κB and TNF-α, whereas phytoestrogens Gen, Res, and Phl, have no such an effect.

Inhibitory effects of genistein and resveratrol on guinea pig gallbladder contractility in vitro.

AIM: To observe and compare the effects of phytoestrogen genistein, resveratrol and 17beta-estradiol on the tonic contraction and the phasic contraction of isolated gallbladder muscle strips and to study the underlying mechanisms. METHODS: Isolated strips of gallbladder muscle from guinea pigs were suspended in organ baths containing Kreb's solution, and the contractilities of strips were measured before and after incubation with genistein, resveratrol and 17beta-estradiol respectively. RESULTS: Similar to 17beta-estradiol, genistein and resveratrol could dose-dependently inhibit the phasic contractile activities, they decreased the mean contractile amplitude and the contractile frequencies of gallbladder muscle strips, and also produced a marked reduction in resting tone. The blocker of estrogen receptor ICI 182780 failed to alter the inhibitory effects induced by genistein and resveratrol, but potassium bisperoxo (1, 10 phenanthroline) oxovanadate bpV (phen), a potent protein tyrosine phosphatase inhibitor, markedly attenuated the inhibitory effects induced by genistein and resveratrol. In calcium-free Kreb's solution containing 0.01 mmol/L egtazic acid (EGTA), genistein and resveratrol inhibited the first phasic contraction induced by acetylcholine (ACh), but did not affect the second contraction induced by CaCl(2). In addition, genistein, resveratrol and 17beta-estradiol also could reduce the contractile responses of ACh and KCl, and shift their cumulative concentration-response curves rightward. CONCLUSION: Phytoestrogen genistein and resveratrol can directly inhibit the contractile activity of isolated gallbladder muscle both at rest and in response to stimulation. The mechanisms responsible for the inhibitory effects probably due mainly to inhibition of tyrosine kinase, Ca(2+) influx through potential-dependent calcium channels (PDCs) and Ca(2+) release from sarcoplasmic reticulum (SR), but were not related to the estrogen receptors.

Differential mechanisms involved in effects of genistein and 17-beta-estradiol on porcine coronary arteries.

The purpose of this work was to examine the differential mechanisms involved in relaxation induced by genistein and 17-beta-estradiol in isolated porcine coronary arteries. Similar to 17-beta-estradiol, genistein could dose-dependently relax 30 mM KCI-precontracted coronary artery rings. The pD2 values of genistein and 17-beta-estradiol were 4.91 +/- 0.13 and 4.98 +/- 0.12 respectively. Incubation with N-L-nitroarginine (L-NNA), endothelium removal or in the presence of a potent inhibitor of protein tyrosine phosphatase sodium orthovanadate did not affect the relaxation induced by genistein, but could partially reduce the vasorelaxation induced by 17-beta-estradiol. The relaxations induced by genistein and 17-beta-estradiol were unaffected by the estrogen receptor antagonist tamoxifen, the inhibitor of prostanoid synthesis indomethacin and the protein synthesis inhibitor, cycloheximide. In addition, both of genistein and 17-beta-estradiol could decrease the contractile responses of KCI, 5-HT and CaCl2, and shift their cumulative concentration-response curves rightward in a parallel manner. These findings suggest that the relaxant effects induced by genistein and 17-beta-estradiol are probably mainly due to inhibition of Ca2+ influx through voltage-dependent calcium channels (VDCCs), and are not related to sex hormone receptor and classical genomic activities. Also there is an interesting finding that the relaxing response of 17-beta-estradiol is partially endothelium-dependent, but that of genistein is not.