Dexmedetomidine on the interplay of IL-6 and STAT3 pathways in adrenal gland damage-induced scalding burns in rats

Scalding burns are a common form of thermal injury that often leads to systemic complications. Pro-inflammatory cytokines like interleukin-6 (IL-6) and the activation of signal transducer and activator of transcription 3 (STAT3) pathways have been linked to the pathophysiology of organ damage caused by burns. This study aimed to investigate the potential therapeutic effects of dexmedetomidine, an alpha 2-adrenergic receptor agonist with anti-inflammatory properties, on the interplay of IL-6 and STAT3 pathways in adrenal gland damage following scalding burns in rats. Twenty-eight rats were divided randomly into four groups. Rats in group 1 (n=7, control) were given only 0.9% intraperitoneal (i.p.) NaCl. Rats in group 2 (n=7, DEX) were exposed to 25 degrees C water for 17 s on day 1 and received 100 mcg/kg/day dexmedetomidine i.p. for 3 days; for rats in group 3 (n=7, Burn), boiling water of 94 degrees C was applied inside for 17 s. Rats in group 4 (n=7, Burn+DEX) were exposed to 94 degrees C water for 17 s and received 100 mcg/kg/day dexmedetomidine i.p. for 3 days. Adrenal gland tissues were histopathological examined, and STAT3, IL-6, and TUNEL staining were performed using immunohistochemically. Our results revealed that scalding burns increased IL-6 and STAT3 expression in the adrenal glands of rats. Histological analysis demonstrated that dexmedetomidine administration ameliorated adrenal gland damage and reduced inflammatory cell infiltration. Our findings suggest that dexmedetomidine protects the adrenal glands in scalding burns. This protection appears to be mediated, at least in part, by its modulation of IL-6 and STAT3 pathways

Comparative analysis of epigallocatechin-3-gallate and TNF-alpha inhibitors in mitigating cisplatin-induced pancreatic damage through oxidative stress and apoptosis pathways

Oxidative stress and inflammation caused by cisplatin, which is frequently used in the treatment of many cancers, damage healthy tissues as well as cancer cells. In this study, we aimed to investigate the effect of epigallocatechin-3-gallate (EGCG) and infliximab (INF) administration on pancreatic endocrine cells in rats treated with systemic cisplatin (CDDP). The rats were randomly divided into 6 groups: group 1 (control group), group 2 (EGCG group), group 3 (CDDP group), group 4 (EGCG + CDDP group), group 5 (CDDP + INF group), and group 6 (EGCG + CDDP + INF group). The study’s findings demonstrated that EGCG and INF effectively reduced the cellular damage induced by CDDP in histopathologic investigations of the pancreas. EGCG and INF, whether used individually or in combination, demonstrated a significant reduction in malondialdehyde (MDA) levels and an increase in glutathione (GSH) levels in the rat pancreas compared to the CDDP group. Immunohistochemically, the enhanced presence of insulin and glucagon positivity in the EGCG and INF groups, along with the absence of TUNEL immunopositivity, indicate that both treatments reduced CDDP-induced apoptosis. Furthermore, the observed lack of immunopositivity in TNF-α and 8-OHdG in the groups treated with EGCG and INF, compared to those treated with CDDP, indicates that these substances can inhibit inflammation. EGCG and INF, whether provided alone or together, can potentially reduce the damage caused to pancreatic islet cells by cisplatin. This effect is achieved through their anti-inflammatory and antioxidant properties during the early stages of the condition

Circadian clock on ionizing radiation-induced testicular injury

Objective: This research focuses on the interaction between the circadian clock and the damage caused to testicular tissue by x-ray ionizing radiation. By examining the links between circadian rhythms and radiation -induced testicular damage, a deeper understanding of the underlying mechanisms may emerge, potentially leading to new strategies to mitigate or prevent such damage and its subsequent consequences. Methods: Twenty-four Sprague-Dawley rats were divided into 3 groups. Rats in group 1 (control group) did not undergo any procedures. Rats in group 2 (day) received 6 Gy total body external x-ray radiation in a single fraction between the hours 05:00 and 06:00. Rats in group 3 (night) received 6 Gy total body external x-ray radiation in a single fraction between the hours 19:00 and 20:00. Results: The day group was compared with the control group, and a decrease in spermatogenetic cells and edematous areas was observed. In addition, there was vacuolar accumulation in the cytoplasm of spermatids in the germinal epithelium and necrotic Leydig cells in the intertubular spaces. In the night group, we observed that the changes observed in group 2 were significantly restored. In terminal deoxynucleotide transferase dUTP nick end labeling and 8-hyd roxy-2'-de oxygu anosi ne immunohistochemical analyses, we observed significantly increased immunopositivity in group 2 compared to the control group and group 3. Conclusion: In conclusion, it reveals that the circadian clock protects against testicular damage caused by x-ray ionizing radiation. By regulating DNA repair processes, antioxidant defense mechanisms, and other important pathways, the circadian clock appears to increase the resistance of testicular tissues to radiation stress

Relationship between overnight dexamethasone suppression test and aging

Background This study aims to investigate the relationship between suppressed cortisol levels measured after the 1-mg dexamethasone suppression test (DST) and age based on the hypothesis that aging can alter the activity of the hypothalamic-pituitary-adrenal (HPA) axis.Methodology Data obtained by the retrospective evaluation of suppressed 1-mg overnight DST results of adults aged >= 18 years with adrenal incidentaloma or suspected endogenous hypercortisolemia between December 2021 and March 2023 were subjected to age-dependent correlation analysis. Individuals aged between 18 and 90 years (n = 1111) were classified into the following four groups: 70 years. DST results were compared according to age groups.Results Median post-DST cortisol was 18.49 nmol/L, with a level of 17.9 nmol/L in females and 20.7 nmol/L in males. The overall rate of DST suppression was 62.7%, with a rate of 63.8% in females and 59.7% in males. On pairwise comparisons of all age groups, there was a difference in post-DST cortisol levels (p = 0.000). Our statistical analysis revealed a strong positive correlation between age and cortisol levels after DST.Conclusions The negative feedback mechanism for cortisol may be altered in older patients. Therefore, the 1-mg DST may yield a higher rate of false positives in the elderly

The effect of anti-tumor necrosis factor therapy on the plasma atherogenic index in rheumatic diseases

Background: The risk of atherosclerosis is increased in individuals with rheumatological disease. The objective of this study is to examine the heightened susceptibility to atherosclerosis in persons afflicted with rheumatological disorders. This study aimed to assess the impact of anti-tumor necrosis factor (anti-TNF) medication on the plasma atherogenic index (PAI) in persons diagnosed with rheumatological disease. Methods: This study used a retrospective cross-sectional design to investigate a cohort of 136 patients with rheumatological disease who were undergoing anti-TNF therapy (Group 1), as well as a comparison group of 117 patients getting conventional therapy (Group 2). Measurements of PAI were conducted at the initial baseline and again at the sixth month of treatment. Results: Initially, there was no statistically significant disparity observed in PAI values between the two cohorts. After a period of 6 months, a notable reduction in PAI was identified in the group receiving anti-TNF medication (P = 0.01), while no significant alteration was detected in the group receiving conventional treatment. Conclusion: It provides findings showing that anti-TNF therapy can reduce the PAI in individuals with rheumatological disease. This may indicate a potential cardiovascular protective effect of anti-TNF therapy