scholarly journals In Vitro Effects of Vitamins C and E on Helicobacter pylori

2021 ◽  
Vol 2 (3) ◽  
pp. 102-106
Author(s):  
Muhammed Kaya ◽  
Alpaslan Tanoğlu ◽  
Züleyha Akkan Çetinkaya ◽  
Efe Serkan Boz ◽  
Hayrunnisa Sezikli ◽  
...  
2021 ◽  
Vol 9 (2) ◽  
pp. 424
Author(s):  
Jianfu Ji ◽  
Hong Yang

Helicobacter pylori is a gastrointestinal pathogen with high prevalence that harms human health. Studies have shown that H. pylori can form antibiotic-tolerant biofilms, which may interfere with the efficacy of clinical antibiotic therapy. Probiotics can antagonize planktonic and biofilm pathogen cells and thus may play an auxiliary role in H. pylori antibiotic therapy. However, the effects of different probiotic strains and antibiotic combinations on H. pylori biofilms need to be further investigated. We determined the cell viability of H. pylori mature biofilms after treatment with Lactobacillus plantarum LN66 cell-free supernatant (CFS), clarithromycin (CLR), and levofloxacin (LVX) alone or in combination by the XTT method. Biofilm cells were observed by scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM). Subsequently, protein and polysaccharide concentrations in biofilm extracellular polymeric substances (EPSs) were quantitatively detected by the Bradford method and the phenol-sulfate method. The results showed that LN66 CFS had an eradication effect on mature H. pylori biofilm. When used in combination with CLR, LN66 CFS significantly attenuated the eradication effect of CLR on biofilms; in contrast, when used in combination with LVX, LN66 CFS enhanced the disrupting effect of LVX. We speculate that the different effects of CFS and antibiotic combinations on biofilms may be related to changes in the content of proteins and polysaccharides in EPS and that the combination of CFS and CLR might promote the secretion of EPS, while the combination of CFS and LVX might have the opposite effect. Accordingly, we suggest that supplementation with L. plantarum LN66 may provide additional help when therapy involving LVX is used for clinical H. pylori biofilm eradication, whereas it may impair CLR efficacy when therapy involving CLR is used.


1996 ◽  
Vol 90 (s34) ◽  
pp. 1P-1P
Author(s):  
ILP Beales ◽  
M Blaser ◽  
L Post ◽  
J Park ◽  
T Yamada ◽  
...  

2009 ◽  
Vol 58 (6) ◽  
pp. 329-335 ◽  
Author(s):  
Yi-Ching Lo ◽  
Yu-Tzu Shih ◽  
Deng-Chyang Wu ◽  
Yi-Chern Lee

Author(s):  
A. R. Crooker ◽  
W. G. Kraft ◽  
T. L. Beard ◽  
M. C. Myers

Helicobacter pylori is a microaerophilic, gram-negative bacterium found in the upper gastrointestinal tract of humans. There is strong evidence that H. pylori is important in the etiology of gastritis; the bacterium may also be a major predisposing cause of peptic ulceration. On the gastric mucosa, the organism exists as a spiral form with one to seven sheathed flagella at one (usually) or both poles. Short spirals were seen in the first successful culture of the organism in 1983. In 1984, Marshall and Warren reported a coccoid form in older cultures. Since that time, other workers have observed rod and coccal forms in vitro; coccoid forms predominate in cultures 3-7 days old. We sought to examine the growth cycle of H. pylori in prolonged culture and the mode of coccoid body formation.


2007 ◽  
Vol 43 (3) ◽  
pp. 121-127
Author(s):  
R. Allem ◽  
FZ. Elkebir ◽  
H. Guetarni
Keyword(s):  

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
HM Lee ◽  
TG Ahn ◽  
CW Kim ◽  
HJ An
Keyword(s):  

1990 ◽  
Vol 64 (03) ◽  
pp. 402-406 ◽  
Author(s):  
M D Oethinger ◽  
E Seifried

SummaryThe present in vitro study investigated dose-, time- and temperature-dependent effects of two-chain urokinase plasminogen activato(u-PA, urokinase) on normal citrated plasma. When 10 μg/ml u-PA wereadded to pooled normal plasma and incubated for 30 min at an ambient temperature (25° C), α2-antiplas-min decreased to 8% of the control value. Incubation on ice yielded a decrease to 45% of control,whereas α2-antiplasmin was fully consumed at 37° C. Fibrinogen and plasminogen fell to 46% and 39%, respectively, after a 30 min incubation at 25° C. Thrombin time prolonged to 190% of control.Various inhibitors were studied with respect to their suitability and efficacy to prevent these in vitro effects. Aprotinin exhibited a good protective effect on fibrinogen at concentrations exceeding 500 KlU/ml plasma. Its use, however, was limited due to interferences with some haemostatic assays. We could demonstrate that L-Glutamyl-L-Glycyl-L-Arginyl chloromethyl ketone (GGACK) and a specific polyclonal anti-u-PA-antibody (anti-u-PA-IgG) effectively inhibited urokinase-induced plasmin generation without interfering with haemostatic assays. The anti-u-PA-antibody afforded full protection ofα2-antiplasmin at therapeutic levels of u-PA.It is concluded that u-PA in plasma samples from patients during thrombolytic therapy may induce in vitro effects which should be prevented by the use of a suitable inhibitor such as GGACK or specific anti-u-PA-antibody.


1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.


1987 ◽  
Vol 58 (03) ◽  
pp. 921-926 ◽  
Author(s):  
E Seifried ◽  
P Tanswell

SummaryIn vitro, concentration-dependent effects of rt-PA on a range of coagulation and fibrinolytic assays in thawed plasma samples were investigated. In absence of a fibrinolytic inhibitor, 2 μg rt-PA/ml blood (3.4 μg/ml plasma) caused prolongation of clotting time assays and decreases of plasminogen (to 44% of the control value), fibrinogen (to 27%), α2-antiplasmin (to 5%), FV (to 67%), FVIII (to 41%) and FXIII (to 16%).Of three inhibitors tested, a specific polyclonal anti-rt-PA antibody prevented interferences in all fibrinolytic and most clotting assays. D-Phe-Pro-Arg-CH2Cl (PPACK) enabled correct assays of fibrinogen and fibrinolytic parameters but interfered with coagulometric assays dependent on endogenous thrombin generation. Aprotinin was suitable only for a restricted range of both assay types.Most in vitro effects were observed only with rt-PA plasma concentrations in excess of therapeutic values. Nevertheless it is concluded that for clinical application, collection of blood samples on either specific antibody or PPACK is essential for a correct assessment of in vivo effects of rt-PA on the haemostatic system in patients undergoing fibrinolytic therapy.


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