Exploring the Antioxidative Effects of Ginger and Cinnamon: A Comprehensive Review of Evidence and Molecular Mechanisms Involved in Polycystic Ovary Syndrome (PCOS) and Other Oxidative Stress-Related Disorders.

Oxidative stress represents the pathophysiological basis for most disorders, including reproductive issues. Polycystic ovary syndrome (PCOS) is heterogeneous endocrine disorder of women characterized primarily by irregular menstrual cycles, hyper-androgenism, and ovulatory dysfunction. In the last decades, PCOS was recognized as a systemic silent inflammation and an oxidative disturbance-related disorder, exerting multifaceted symptoms, including metabolic. PCOS treatment should involve a personalized approach tailored to individual symptoms; however, the results are often unsatisfactory. Various supplementary treatments have been proposed to assist in the management and alleviation of PCOS symptoms. Cinnamon and ginger, known for millennia as herbs used in spices or traditional medicine for the treatment of various diseases, are of interest in this study. The aim of this study is to evaluate and investigate the effects of cinnamon and ginger in PCOS patients. Using relevant keywords we searched through PubMed/MEDLINE, Science Direct, Google Scholar and Web of science to find animal studies, pre-clinical, and clinical studies which were then reviewed for usage. Out of all of the reviewed studies a total of 65 studies were included in this review article. Cinnamon and ginger can affect hormonal status, lipid profile, obesity, and insulin resistance by mitigating oxidative stress and inflammation. Generally, based on current clinical evidence, it was revealed that supplementation with cinnamon or ginger had a useful impact in patients with PCOS. This review summarizes the antioxidative effects of ginger and cinnamon in PCOS treatment, highlighting their potential benefits in other oxidative stress-related pathologies.

Potential factors of Helicobacter pylori resistance to clarithromycin.

OBJECTIVES: A comparative dissolution kinetics test (CDKT) and bioequivalence studies of generic proton pump inhibitors (PPIs) do not model pharmacological acid suppression (PAS) and pathological duodenogastric reflux (PDGR). This study aimed to model them in CDKT to assess drugs stability and potential pantoprazole-clarithromycin interactions. METHODS: In CDKT, PDGR (dissolution medium pH 7.00 ± 0.05, preexposure at pH 1.20 ± 0.05) and PAS (pH 4.00 ± 0.05) were modelled for original pantoprazole (OP) and its generics (GP1-4). In CDKT with high-performance liquid chromatography, dissolution gastric medium in adequate (pH 4.00 ± 0.05) and inadequate (pH 1.20 ± 0.05) PAS were modelled for original clarithromycin (OC) and its generics (GC1-4). RESULTS: After exposure in pH 7.00 ± 0.05, pantoprazole was released from GP1 within 10 min in the amount of 68.8%. In рН 4.00 ± 0.05, 83.0% and 81.5% of pantoprazole were released from GP1 and GP4. When OP, GP2 and GP3 were placed in pH 7.00 ± 0.05, pantoprazole was released in amount: 99.4%, 88.0% and 98.2%. Clarithromycin releasing from OC, GC1, GC2, GC3, GC4 in pH 4.00 ± 0.05 was 93.5%, 91.6%, 92.9%, 79.4% and 83.0%. In pH 1.20 ± 0.05: 9.7%, 6.7%, 8.5%, 33.3%, 28.8%. CONCLUSIONS: Destruction of enteric coats of some local pantoprazole generics in CDKT-models might be a potential factor for inadequate therapy.