Prosopis farcta, a medicinal plant of the Fabaceae family, is being explored scientifically on the basis of its diverse biological activities and medicinal importance. Rich in flavonoids, alkaloids, and phenolics, P. farcta exhibits strong antioxidant, anti-inflammatory, antimicrobial, and hepatoprotective activities. It has been demonstrated that it can exert neuroprotection by modulating oxidative stress and inflammatory pathways. Further, P. farcta possesses antidiabetic activity through the facilitation of the insulin sensitivity and glucose metabolism, and hence it is a good candidate for glycemic control. Its wound healing efficacy via the anti-inflammatory and antimicrobial activities has been studied through in-vivo and in-vitro models. P. farcta also possesses cardioprotective activity via lipid metabolism modulation and improvement of endothelial function. Nevertheless, while P. farcta fruit extracts have hepatoprotective effects, evidence further suggests the potential for hepatotoxicity with its seed extract, emphasizing dose-dependent analysis. Despite its therapeutic pharmacological potential, additional clinical trials must determine its safety profile, define its optimal therapeutic dosages, and clarify its particular molecular mechanisms of the action. This review consolidates the current evidence in support of the medicinal worth of P. farcta, demonstrating its applications in modern medicine.

The cyclic GMP–AMP synthase–stimulator of interferon genes (cGAS–STING) signaling pathway is a central component of innate immunity that senses cytosolic double‑stranded DNA and initiates type I interferon and inflammatory responses. Controlled activation of this pathway is essential for antimicrobial defense and antitumor immune surveillance. In contrast, dysregulated or persistent signaling can promote chronic inflammation, tissue damage, autoimmune disorders, or immune evasion in cancer and infectious diseases. Therefore, tight regulation of cGAS–STING activity is critical for maintaining immune homeostasis. MicroRNAs (miRNAs) have emerged as key post‑transcriptional regulators that fine‑tune cGAS–STING signaling by directly targeting core pathway components or indirectly modulating related immune signaling molecules. This article provides a comprehensive review of current evidence describing miRNA‑mediated regulation of the cGAS–STING axis across diverse pathological contexts, including malignancies, viral and bacterial infections, and autoimmune or inflammatory diseases. In various cancers, miRNA‑mediated suppression of this pathway contributes to reduced interferon signaling, immune escape, therapy resistance, and tumor progression, although in certain cellular settings, controlled inhibition of cGAS–STING may exert protective or antitumor effects. During infectious diseases, some miRNAs are exploited by pathogens to attenuate innate immune sensing, whereas others enhance host defense by modulating negative regulators of immune signaling. In autoimmune and inflammatory disorders, dysregulated miRNA expression can either restrain excessive inflammation or exacerbate disease progression. Overall, this review underscores the miRNA–cGAS–STING regulatory axis as a dynamic and context‑specific network with broad relevance across human diseases.

Objective: Oxidative stress plays a key role in the pathogenesis of rheumatoid arthritis (RA). Glutathione peroxidase (GPx) is a peroxidase enzyme that defends mammalian cells against oxidative stress.  The Pro198Leu polymorphism of the GPx-1 gene, has been reported to influence its activity. This study aimed to investigate the association of this polymorphism with RA risk in an Iranian population.

Methods: In this case-control study, 45 RA patients and 45 healthy controls were enrolled. Genomic DNA was extracted from blood samples, and genotyping for the Pro198Leu polymorphism was performed using the PCR-RFLP technique. Statistical analysis was conducted using SPSS software, employing chi-square tests and ANOVA.

Results: The mean age of all participants was 55.69 years. Genotype distribution was as follows: CC (50.0%), CT (44.4%), and TT (5.6%). Chi-square analysis revealed no significant difference in genotype frequencies between patients and controls (p = 0.779). Furthermore, no significant association was found between genotypes and age or gender. All groups were in Hardy-Weinberg equilibrium.

Conclusion: The findings indicate that the GPx-1 Pro198Leu polymorphism is not significantly associated with the risk of developing RA in the studied population.

Background: Inflammation is involved in development of age-related macular degeneration (AMD), with the cGAS-STING pathway playing a critical role. This pathway activates in response to cytosolic DNA, such as accumulated mitochondrial DNA from aging or oxidative stress. Given STING's encoded by the STING1 gene, we hypothesized that functional STING1 polymorphisms might influence AMD susceptibility.

Methods:  To identify the most relevant polymorphism, all polymorphisms of STING1 with MAF ≥1% were extracted from NCBI. The rs7380824 was selected for genotyping as it demonstrated the highest PSI value—a novel metric combining CADD score and MAF—indicating high potential deleteriousness. Then a hospital-based case-control study comprised 237 subjects (122 AMD patients, 115 controls) was carried out to investigate the association between the rs7380824 and the risk of AMD. Genotyping employed PCR-RFLP, and statistical analyses used logistic regression adjusted for age, smoking, and workplace exposure.

Results: The genotypic frequency of the rs7380824 polymorphism was in Hardy-Weinberg equilibrium. No significant association was found between the genotypes of this polymorphism and AMD risk. However, a borderline protective effect was observed for the TT genotype versus CC+CT (OR=0.19, 95% CI: 0.03-1.16, p=0.073) after adjusting for age, workplace and smoking habits of the participants.

Conclusion: As the first investigation of the association between the STING1 polymorphism (rs7380824) and AMD risk, this study did not identify a significant overall association. However, the observed protective effect of the TT genotype, potentially covered by the limited sample size, highlights the necessity for validation in studies with larger samples.

Objective: Childhood obesity is a global health concern associated with long-term metabolic complications. MicroRNA-135b (miR-135b) has been implicated in regulating adipogenesis, glucose metabolism, and insulin signaling, partly by directly targeting SIRT1, a key metabolic regulator that plays a crucial role in energy homeostasis and inflammation. However, the role of miR-135b in pediatric obesity remains unclear. This study aimed to investigate circulating miR-135b level and its relationship with SIRT1 expression, lipid profile, and glycemic parameters in children and adolescents with obesity.

Methods: A total of 67 participants (36 obese and 31 normal-weight controls) aged 8–16 years were enrolled. Anthropometric measurements and biochemical analyses were performed. miR-135b and SIRT1 expression levels were measured using quantitative real-time PCR. Insulin resistance was assessed using HOMA-IR, and metabolic syndrome was diagnosed based on International Diabetes Federation criteria.

Results: miR-135b expression was significantly elevated in the obesity group compared to controls and was highest among participants with insulin resistance and metabolic syndrome. Elevated miR-135b correlated positively with BMI z-score, insulin levels, HOMA-IR, total cholesterol, triglycerides, and LDL-C, while showing no significant correlation with HDL-C. In contrast, SIRT1 expression was significantly decreased in obese individuals (p = 0.0026) and inversely correlated with miR-135b levels.

Conclusion: Elevated miR-135b and reduced SIRT1 expression are associated with obesity-related metabolic disturbances in children and adolescents. These findings suggest that the miR-135b/SIRT1 axis may play a pivotal role in the development of insulin resistance and dyslipidemia, highlighting miR-135b as a potential biomarker and therapeutic target for early intervention in pediatric obesity.

Objectives: Dyslipidemia and oxidative stress have been reported to play important roles in the pathogenesis of type 2 diabetes mellitus (T2DM) complications. This study aimed to test the hypothesis whether curcumin supplementation combined with aerobic exercise could prevent dyslipidemia and oxidative stress in a rat model of T2DM.

Methods: Male Wistar rats with nicotinamide-streptozotocin-induced T2DM were divided into four groups including untreated diabetes, diabetes treated with curcumin (30 mg/kg, three times weekly), diabetes treated with aerobic exercise (4-week progressive treadmill training), and a combination group. Also, healthy control groups (untreated, curcumin-treated, and curcumin + aerobic-treated) were studied to determine the side effects of the treatments. Fasting blood sugar (FBS), lipid profiles (triglycerides, total cholesterol, LDL, HDL) and antioxidant enzyme activities (catalase, SOD, GPx) were measured by commercial kits after 4 weeks of treatment protocol.

Results: Diabetic rats had significantly elevated serum levels of FBS, triglycerides, total cholesterol, LDL, and reduced antioxidant activities compared to controls. Curcumin and aerobic exercise alone improved these parameters significantly, but their combination was more effective in reducing FBS, improving lipid profiles, and boosting antioxidant activities.

Conclusion: The combination of curcumin and aerobic exercise has more potential to ameliorate dyslipidemia and oxidative stress in T2DM rats, compared to treatments individually. These findings require further exploration in clinical settings.

Objectives: Zinc (Zn) is a vital trace element, and its accurate measurement in biological samples is important for diagnosing Zn deficiency. However, the difference in Zn concentration between serum and plasma samples and the effect of anticoagulants on results are major methodological challenges. The aim of this study was to compare the effect of common anticoagulants (EDTA, citrate and heparin) on Zn concentration in blood samples using a routine colorimetric method.

Methods: This research was conducted on 20 healthy volunteers (10 women and 10 men). Samples of serum, EDTA, citrate and heparin plasma were collected and Zn levels were measured using a routine colorimetric method based on 5‑Br‑PAPS.

Results: The results of this study showed that Zn concentrations in EDTA‑ and citrate‑anticoagulated plasma were significantly lower than those measured in serum (P<0.05). In contrast, no statistically significant difference was observed between serum and heparin‑anticoagulated plasma (P>0.05). Spearman’s correlation analysis showed a strong positive correlation between serum Zn concentrations and those measured in heparin (r=0.831, P<0.001) and citrate (r=0.704, P<0.01) plasma samples, whereas the correlation between serum and EDTA plasma was positive but weak and not statistically significant (r=0.099, P>0.05).

Conclusion: The choice of anticoagulant is a critical pre-analytical factor in Zn measurement using colorimetric methods. These findings show that chelating anticoagulants like EDTA and citrate spuriously lower Zn concentration, whereas heparin‑anticoagulated plasma yields Zn measurements that are comparable to those obtained in serum. These results are of great importance for the accurate interpretation of results in clinical laboratories.

Objectives: The genetic and environmental factors have crucial role in colorectal cancer (CRC) pathogenesis. Due to important role of proline , glutamic acid, and leucine-rich protein 1 (PELP1)    and c-Src genes in different types of malignancy, this study aimed to investigate the expression levels of the PELP1 and c-Src genes in tumor versus matched non-cancerous margin tissues of patients with CRC, and further evaluate their capacity as potential diagnostic biomarkers.

Methods: The gene expression of PELP1 and c-Src in 31 tumor tissues and 31 non-cancerous margin tissues of CRC subjects was analyzed by the Real-Time PCR. Moreover, Receiver Operating Characteristic (ROC) curve analysis was utilized for the determination of these genes' RNA levels as potential biomarkers.

Results: Our findings indicated the increased PELP1 (P=0.016) and c-Src (P=0.006) gene expression in tumor tissues, compared to non-cancerous margin tissues in CRC. The result of ROC analysis showed that the area under the curve (AUC)  for PELP1 and c-Src were 0.673 (Cut off:7.74, sensitivity:0.714, specificity:0.615) and 0.731 (Cut off:16.04, sensitivity: 0.857, specificity: 0.653), respectively.

Conclusion: The higher expression of c-Src and PELP1 genes in tumor tissues compared to non-cancerous margin tissues indicated that these genes are critical components of the signaling pathways involved in CRC pathogenesis. Furthermore, the findings revealed that studied genes can have a potential for diagnosis purposes in CRC.