Background/Objectives: Diabetic cardiomyopathy is a distinct myocardial dysfunction characterized by structural and functional changes in the heart that occur in diabetic patients independently of coronary artery disease or hypertension. It is closely associated with oxidative stress, inflammation, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress, and contributes to progressive cardiac damage. This study aimed to evaluate the cardioprotective effects of dapagliflozin (DAPA) and trimetazidine (TMZ) in a rat model of doxorubicin-induced cardiomyopathy with streptozotocin-induced diabetes, focusing on their potential mechanisms related to ER stress. Methods: A total of 48 Sprague Dawley rats aged 6–8 weeks were randomly distributed equally into six cages. The diabetes model was induced by intraperitoneal administration of streptozotocin (STZ) and rats with blood glucose levels above 250 mg/dL were considered diabetic. For those rats with diabetes, cardiotoxicity was induced by intraperitoneal injection of 5 mg/kg/week doxorubicin (DOXO) for 4 weeks. After a cumulative dose of 20 mg/kg doxorubicin, a week break was given, followed by the administration of TMZ (10 mg/kg) and/or DAPA (10 mg/kg) to the treatment groups. Results: STZ administration caused diabetes and significant degeneration in cardiomyocytes. With the addition of DOXO (STZ + DOXO), cardiomyocyte degeneration became more severe. When the study groups were histopathologically evaluated based on parameters of degenerative cardiomyocytes, vascular congestion, and edema, it was shown that both TMZ and DAPA, whether applied alone or in combination, reduced damage in heart tissue. Both TMZ and DAPA reduced cardiomyocyte damage, and their combination provided the lowest level of damage through the reduced ER stress pathway by reducing GRP 78 and CHOP positivity. Conclusions: TMZ and DAPA reduce ER stress and have protective effects against diabetic-induced cardiotoxicity. Combination therapy or TMZ was found to be more effective than DAPA in alleviating ER stress. Combination therapy appears to carry potential effects for reducing cardiac cell damage in individuals with diabetes.
Acute liver injury is an increasing global health problem. It is a widespread side effect of cisplatin treatment in the clinic and can lead to liver failure if not treated promptly. Previous studies have revealed that green tea can protect some organs from treatments. However, the potential of white tea to prevent the negative effects of acute liver injury has not been addressed so far. The purpose of this study was to investigate the reduction in cisplatin-induced liver injury in rats receiving white tea. Female Sprague Dawley rats with similar weight were selected in this study. Twenty-four rats were divided into three groups of eight animals each and ad libitum nutrition was provided. The control and cisplatin groups were given tap water only, while the white tea + cisplatin group received white tea at a 0.5% weight/volume concentration for four weeks. At the end of the fourth week, the white tea + cisplatin group and the cisplatin group received a single dose of cisplatin (7 mg/kg) via the intraperitoneal route. Five days after that procedure, the rats were anesthetized. Liver tissues and blood samples were collected, which were used for biochemical and histopathological analyses. According to biochemical results, liver tissue MDA and GSH, serum ALT, and AST levels significantly increased in the cisplatin group compared to the control group. Compared with the cisplatin group, although MDA, AST, ALT, and GSH levels were lower in the white tea + cisplatin group, only GSH levels were statistically different. The examination of histopathological and immunohistochemical findings revealed apoptotic cells, vascular congestion, and sinusoidal dilatation in the cisplatin group compared to the control group. This adverse event decreased in the white tea + cisplatin group compared to the cisplatin group. In conclusion, white tea exhibits an ameliorating effect on cisplatin-induced liver injury.
Background and Objectives: Obesity and related disorders are an increasing global health problem. Achieving and maintaining long-term weight loss through lifestyle changes and/or pharmacological interventions have not met expectations. Dietary supplements and alternative treatments have also shown limited effectiveness in this regard. The consumption of green tea in general has been shown to benefit obese patients, with effects attributed to caffeine, catechins, polyphenols and other components. However, the potential of white tea to prevent and treat the negative effects of obesity has not been addressed so far. In this study, the effect of white tea (WT) consumption in obese individuals was anthropometrically and biochemically investigated. Materials and Methods: Based on anthropometric and biochemical assessments, the patients were assigned to the control, orlistat, metformin and WT groups. Patients were given a diet and exercise program and one of either orlistat, metformin or WT for 12 weeks. At the end of the 12th week, the anthropometric and biochemical measurements were reassessed. Results: Body weight, waist circumference and BMI parameters decreased significantly in all groups. TNF-α, IL-6, IL-1β and MMP-9 levels decreased significantly in the WT group. In addition, contrary to a significant elevation in HDL-C, the serum cholesterol, LDL-C and TG levels decreased significantly. Furthermore, leptin, ghrelin and asprosin levels decreased significantly. Serum glucose levels decreased significantly in all groups except for the control. In the WT group, while there was a significant decrease in the levels of serum PL MDA and 8-OHdG, the opposite was true for GSH. Conclusions: The oral consumption of WT, its availability and its potency in obesity treatment and prevention pave the way for further delineation of the mechanisms of actions of its bioactive compounds at the cellular and endocrinological levels.
There is an increasing occurrence of periodontitis and metabolic syndrome (MetS), which is resulting in a decline in the overall quality of life. Both disorders can occur together since they are both linked to insulin resistance and systemic inflammation. However, evidence for a role of interleukin (IL)-20 in this comorbidity is very limited. This cross-sectional study aimed to comprehensively investigate, for the first time, the levels of RANKL/OPG, MMP-8 and OSI as well as the role of IL-20 in patients with MetS and periodontitis. The study included a total of 80 individuals, divided into four groups: 20 individuals who were healthy both systemically and periodontally, 20 individuals who were systemically healthy but had periodontitis, 20 individuals who had MetS but were periodontally healthy, and 20 individuals who had both MetS and periodontitis. Periodontal clinical parameters (plaque index, gingival index, bleeding on probing, clinical attachment loss, probing pocket depth) were evaluated. Gingival crevicular fluid (GGF) and serum samples were collected and used for biochemical assays. Enzyme-linked immunosorbent assay was used to determine the levels of IL-20, receptor activator of nuclear factor kappa B ligand (RANKL)/osteoprotegerin (OPG), matrix metalloproteinase-8 (MMP-8) and oxidative stress index (OSI). IL-20 levels measured in serum and GCF were statistically significantly highest in patients with MetS and periodontitis (p = 0.001). Significant positive correlation was observed between serum and GCF IL-20 values and periodontal parameters (p < 0.05). There was a positive correlation between RANKL and RANKL/OPG levels and IL-20 and clinical parameters (p < 0.05). OSI values were found to be increased in the presence of both periodontitis and MetS (p = 0.001) and were positively correlated with serum and GCF IL-20 (p < 0.05). These data from the study suggest a correlation between IL-20 and both MetS and periodontitis. IL-20 may potentially worsen the condition of periodontal tissue by increasing both the oxidative stress levels, periodontal collagen degredation and the ratio of RANKL to OPG. This study was registered on ClinicTrials.gov (NCT06092853), 2023-10-10, retrospectively registered.
This book, Epigallocatechin-3-Gallate (EGCG): From Biochemical Pathways to Physiological Outcomes, contains four chapters that detail epigallocatechin gallate (EGCG), a compound found in tea leaves, its effects on health, and future directions. Chapter 1 discusses the tea plant (Camellia sinensis L), the process of tea production, the types of tea, and the components found in tea. Chapter 2 focuses on EGCG, a highly potent polyphenolic compound present in tea that exhibits a broad spectrum of biological effects on human health. Chapter 3 expands on EGCG, arguing that EGCG is better understood as a distributed, network-level regulator acting simultaneously across the gut–liver axis, neuro–immune crosstalk, cardiovascular–renal–endocrine integration, and cellular senescence rather than as a compound with one dominant molecular target. Finally, chapter 4 discusses the gap between EGCG's clinical translation as a network-level regulator of redox, inflammatory, and metabolic signaling, and argues that this gap may reflect not simply a deficiency in biological efficacy but an incomplete match between EGCG's context-dependent pharmacology and the single-target, fixed-exposure assumptions of conventional translational pharmacology.