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Introduction / objective: Fibromyalgia syndrome (FMS), affecting 3–10% of the population, presents a challenge due to its complex symptomatology. Mitochondrial miRNAs (mitomiRs) are highlighted for their significant role in metabolic disorders. This study aimed to assess demographic data in Primer FMS patients and explore potential targets through mitomiR profiling. Methods: In our study, we examined 17 FMS patients and 18 controls, chosen based on specific criteria. Mitochondria were isolated from PBMCs in patient/control blood samples using the MACS method. Mitochondrial purity was verified through RT-qPCR and Western Blot. Following this, we extracted microRNAs and analyzed the levels of 3 mitochondrial miRNAs linked to oxidative stress (mitomiR-145-5p, mitomiR-23a-3p, mitomiR-223-3p) using RT-qPCR. Results: It was found that pain (P < 0.0001), fatigue (P = 0.0005), sleep quality (P < 0.0001), and depression (P < 0.0001) scores were significantly different in the FMS patient group compared to the control group. But the average BMI values have no difference compared to the control group (p = 0.7473). For the first time, a significant increase in mitomiR-145-5p was observed in the PBMCs of FMS patients compared to the control group (p = 0.0010). There was no significant difference observed in the gene expression levels of mitomiR-223-3p (p = 0.1623) and mitomiR-23a-3p (p = 0.4897). Conclusion: We demonstrated that mitomiR-145-5p plays a significant role in the progression of FMS pathology. Our study offers new insights, suggesting that mitochondrial miRNAs may have roles in FMS patients, which has not been previously investigated in the literature, thus providing a fresh perspective on the condition. [ABSTRACT FROM AUTHOR]

The present study aimed to examine the protective effect of quercetin (QUE) on cyclophosphamide (CTX)-induced nephrotoxicity. For that purpose, 24 mice were divided into four groups (Control, QUE, CTX, and CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg of cyclophosphamide on the 1st and 7th days. The QUE and CTX + QUE groups were treated with 50 mg/kg of quercetin daily for 14 days. At the end of the experiment, the animals were sacrificed, and kidney samples were analyzed. The results indicated that CTX leads to severe morphological degenerations and disruption in renal function. Serum BUN, Creatinine, Uric acid, tissue Bax, Caspase 3, TNF-α and IL-1β expression levels were upregulated in the CTX group compared to Control and QUE groups (p < 0.05). Although MAPK/ERK phosphorylation level is not affected in CTX group, there was a significant increase in CTX + QUE group (p < 0.05), but the NF-κB was significantly suppressed in this group (p < 0.01). The RT-qPCR results showed that the cyt-c and the Bax/Bcl-2 ratio mRNA expression folds were upregulated in the CTX group (p < 0.01), which was downregulated in the CTX + QUE group. However, there was a significant difference in the CTX + QUE group compared to the Control and QUE groups (p < 0.01). The findings showed that administering quercetin along with cyclophosphamide alleviated renal injury by regulating apoptotic and inflammatory expression. Moreover, the administration of quercetin and cyclophosphamide could synergistically improve renal function test results, and activate cellular responses, which upmodulate MAPK/ERK phosphorylation and suppression of NF-κB. Twenty-four mice were equally divided into 4 groups (Control, QUE, CTX, CTX + QUE). CTX (1). CTX + QUE groups received 200 mg/kg Cyclophosphamide at 1st and 7th days of study (2). Animals in QUE and CTX + QUE received 50 mg/kg quercetin daily for 14 days (3). All animals were euthanized (4) and kidney samples were used for microscopic, western blotting and RT-qPCR analysis (5). Cyclophosphamide exposure increased expression of inflammatory (6) TNF-α, IL-1β, and (7) pro-apoptotic Bax, Caspase 3, cyt-c, and gold standard Bax/Bcl-2 ratio. Quercetin treatment alleviated inflammatory cytokine (8) and apoptotic protein expression levels (9). This process might be modulated through increased MAPK/ERK phosphorylation level which potentially regulate the suppression process of NF-κB level (10). [ABSTRACT FROM AUTHOR]

Background: Multiple Sclerosis (MS) is an inflammatory, demyelinating and neurodegenerative disease. In this study, we investigated serum protein levels of Interleukin-13 (IL-13) and Interleukin-22 (IL-22) cytokines. These cytokines play an important role in the generation and regulation of the inflammatory response, which is the pathogenesis of MS, and are potential biomarkers for monitoring therapeutic response. cytokines may play a role in the development of MS lesions. Methods: The study included 66 MS patients and 22 healthy individuals. IL-13 and IL-22 cytokine protein levels were measured by ELISA from peripheral blood serum samples collected from the participants. Patient demographics and treatment history data were also collected. Results: IL-13 and IL-22 parameters were lower in MS patients compared to the control group. There was a significant difference between the patient and control groups in terms of IL-13 (p<0.001). Although the mean IL-22 level of the control group was higher than the patient group, the difference did not reach a significant level (p: 0.257). Conclusion: The results of the study suggest that IL-13 and IL-22 cytokines play an important role in the pathogenesis of MS and are affected by fingolimod and glatiramer acetate treatment. [ABSTRACT FROM AUTHOR]

Ovarian cancer is one of the most common malignancies in the female reproductive system. Honey has a range of medical properties. It has been shown to have anticancer properties, especially for breast, cervical, etc. cancers.In our study, we aimed to investigate the cytotoxic, anti-migratory, and mitochondrial apoptotic pathway effects of Multifloral honey on the Ovarian Adenocarcinoma SKOV3 cell line.The MTT assay was used to evaluate the anti-proliferative effect of Multifloral honey on SKOV3 and HDF cell lines. Subsequently, differences in the expression of genes involved in mitochondrial apoptosis in the SKOV3 cell were examined using RT-qPCR and Western Blot methods. Finally, the effects of Multifloral honey on migration in SKOV3 cell were observed under a microscope.It was found that honey did not exhibit a cytotoxic effect on HDF cell, but significantly suppressed SKOV3 cell proliferation, promoting apoptosis. In our study on SKOV3 cells, we observed a significant decrease in the ratio of apoptotic genes Bax/Bcl-2 (P = 0.0043) using the RT-qPCR method, while the expressions of Cyt-C and Bad increased significantly (P = 0.0034 and P < 0.0001, respectively). Western Blot analysis confirmed the decrease in the Bax/Bcl-2 ratio. In our wound healing results, we found that honey inhibited migration in the SKOV3 cell.Our results provide preliminary evidence that Multifloral honey induces cell death in SKOV3 cell line through involvement in the intrinsic apoptotic pathways, and it demonstrates significant anticancer activity against human ovarian cancer cell lines for the first time. [ABSTRACT FROM AUTHOR]

Background: Chemotherapy drugs may lead to hepatic injury, which is considered one of the limitations of these drugs., Objectives: The aim of this study was to evaluate the effect of quercetin (QUE) on M1/M2 macrophage polarization and hepatoprotective effect in cyclophosphamide (CTX)-induced liver toxicity., Methods: Twenty-four mice were divided into four groups (Control, QUE, CTX, CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg CTX. The animals in the QUE and CTX + QUE groups received 50 mg/kg QUE. All animals were sacrificed, and serum and liver samples were used for laboratory analyses., Results: Examinations indicated that CTX exposure led to disruption of liver functions and morphological degenerations. Tissue pro-apoptotic Bax and caspase 3, pro-inflammatory TNF-α and IL-1β, transcription factor NF-κB, and M1 macrophage polarization marker CD86 were upregulated significant (p < 0.05) in this group. In addition, CTX exposure led to significantly (p < 0.05) upregulation of the Bax/Bcl-2 mRNA ratio and DNA fragmentations. The PCNA-positive hepatic cell ratio and anti-apoptotic Bcl-2 expression are remarkably suppressed (p < 0.05). Immunohistochemical analyses are also indicated that M2 macrophage polarization marker CD163 is slightly but remarkably (p < 0.05) downregulated in the CTX group compared to the Control and QUE groups. The morphological and biochemical disruptions were alleviated in QUE-treated animals in the CTX + QUE group. Liver function test results, apoptosis, inflammatory, transcription factor NF-κB, regeneration/proliferation, and apoptotic index results in this group were similar (p > 0.05) to the control and QUE groups. The M1 cell surface marker expression of CD86 is significantly (p < 0.05) downregulated, and M2 macrophage polarization marker expression of CD163 is upregulated significantly (p < 0.05) compared to the CTX group., Conclusions: This study indicates that QUE has the potential to downregulate CTX-induced hepatic injury and regulate M1/M2 macrophage polarization to the M2 side, which indirectly demonstrates activation of anti-inflammatory signalling and tissue repair., (© 2025 The Author(s). Veterinary Medicine and Science published by John Wiley & Sons Ltd.)