These results suggest that L. plantarum XB7 produces secreted factors capable of modulating inflammation during H. pylori infection, and this probiotic Lactobacillus strain shows promise as an adjunctive therapy for treating H. pylori-associated disease.
Background and Aim
Helicobacter pylori is a class I carcinogen. Nowadays, the problem of antibiotic resistance is increasing worldwide. The latest prevalence rates of infection and resistant status in Thailand vary or are out of date. Our aims are to identify the current prevalence and antibiotic resistance patterns in Thailand and to suggest regimens for treatment‐naive and ‐resistant patients.
Methods
This descriptive retrospective study was conducted, using a urea breath test, on patients in King Chulalongkorn Memorial Hospital between 2013 and 2017. They were categorized into the diagnostic group and posttreatment group. Specimens from some patients were cultured to identify the antibiotic‐resistant pattern.
Results
There were 1894 patients included in our study. The prevalence of H. pylori infection in dyspeptic patients was 28.4%. Of 1258 patients, 1165 (92.61%) responded to initial treatment. The 95 patients who failed to respond could respond to second‐line treatment of longer period, at higher doses, or using other antibiotics (success rate 68.42%). There were 21.43, 14.29, and 10.71% of patients resistant to ciprofloxacin, metronidazole, and clarithromycin, respectively. However, no patients resistant to amoxicillin, tetracycline, and levofloxacin were found.
Conclusion
The prevalence of H. pylori infection in Thailand has increased slightly. Initial regimens (triple therapy or sequential therapy or quadruple therapy) can be effective for the eradication of H. pylori infection, with a success rate of > 90%. For patients who failed to respond to initial triple therapy, using a longer duration of triple therapy or changing to quadruple therapy could be a good alternative. The resistance rates of amoxicillin, metronidazole, levofloxacin, and tetracycline are declining, but those of clarithromycin and ciprofloxacin are increasing.
The aim of this study was to evaluate the protective effects of genistein on lipid accumulation and apoptosis in estrogen deficient rats with NASH. Female Sprague–Dawley rats (n = 48) were divided into ovariectomized (OVX) and non-OVX groups. Each group was then sub-divided into 3 subgroups; control, NASH (rats fed with a high-fat, high-fructose (HFHF) diet), and NASH+Gen (rats fed with HFHF diet plus daily genistein at 16 mg/kg BW). Results showed that HFHF diet induced liver fat accumulation in both non-OVX and OVX rats, which was evidenced by hepatic steatosis on liver pathology and increased hepatic free fatty acid (FFA) and triglyceride levels. Hepatic fat accumulation was significantly more severe in NASH rats with OVX than non-OVX. Hepatocyte apoptosis was more severe in NASH groups compared with that in control groups. Genistein administration significantly improved histopathology of NASH in both non-OVX and OVX rats and attenuated hepatic lipid accumulation, oxidative stress, and hepatocyte apoptosis. Genistein also down-regulated PPARγ and up-regulated adiponectin expression. In summary, NASH could be worsened by estrogen deficiency, indicating the protective action of estrogen on NASH. Genistein administration alleviated hepatic steatosis and apoptosis through the down-regulation of PPARγ and up-regulation of adiponectin expression.
Nonalcoholic steatohepatitis (NASH) has become a global chronic liver disease, but no effective medicine has been proven to cure it. This study investigated the protective effects of genistein, a phytoestrogen, on NASH and examined whether it has any effect on hepatic PPARγ. Male Sprague-Dawley rats were divided into four groups: control group fed ad libitum with standard rat diet, NASH group fed ad libitum with high-fat diet to induce NASH and NASH + Gen8 group and NASH + Gen16 group fed with high-fat diet plus intragastric administration of 8 or 16 mg/kg genistein once daily. After 6 weeks, liver samples were collected to determine MDA, TNF-α, PPARγ, and histopathology. The findings were that levels of hepatic MDA and TNF-α increased in NASH group, but 16 mg/kg genistein reduced these levels significantly. Downregulation of hepatic PPARγ was observed in NASH group, but genistein significantly upregulated the expression of PPARγ in both NASH + Gen groups. The histological appearance of liver in NASH group presented pathological features of steatohepatitis which were diminished in both NASH + Gen groups. The results suggest that genistein attenuates the liver histopathology of NASH with upregulation of hepatic PPARγ, reduction of oxidative stress, and inhibition of inflammatory cytokine.
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