Circulating levels of C1q/TNF-α-related protein 6 (CTRP6) in coronary artery disease and its correlation with inflammatory markers.

Introduction: Circulating levels of C1q/TNF-α-related protein 6 (CTRP6) is an adipokine that is involved in regulation of glucose and lipid metabolism, inflammation, and insulin sensitivity. However, the exact role of CTRP6 in metabolic processes remains unclear due to conflicting findings. To address current gap, we aimed to investigate the serum levels of CTRP6 in patients with coronary artery disease (CAD) and its association with inflammatory cytokines. Method: In this case-control study, the serum levels of CTRP6, interlukin-6 (IL-6), tumor necrosis factor- α (TNF-α), adiponectin, and fasting insulin were measured using enzyme-linked immunosorbent assay (ELISA) kits in a total of 176 participants, consisting of 88 CAD patients and 88 control subjects. Additionally, various anthropometric and biochemical measurements were measured and compared between cases and controls. Results: The present study found that serum levels of CTRP6 were significantly higher in the CAD group (561.3 ± 15.14) compared to the control group (429.3 ± 12.85, p < 0.001). After adjusting for age, sex, and body mass index (BMI), CTRP6 levels were found to be positively associated with the risk of CAD (p < 0.001). Correlation analysis in CAD subjects revealed a positive correlation between CTRP6 levels and BMI, systolic blood pressure (SBP), malondialdehyde (MDA), TNF-α, and IL-6, as well as a negative correlation with creatinine and total anti-oxidant capacity. Conclusion: The findings of this study provide novel evidence that elevated serum levels of CTRP6 are significantly associated with an increased risk of developing CAD. Moreover, our results indicate a correlation between CTRP6 and various risk factors for atherosclerosis. Supplementary Information: The online version contains supplementary material available at 10.1007/s40200-024-01415-5.

A positive correlation of serum SFRP1 levels with the risk of developing type 2 diabetes mellitus: a case-control study.

OBJECTIVE: Secreted frizzled-related protein 1 (SFRP1) is an adipokine whose production is significantly altered in metabolic disorders. Considering the relationship between dysfunction of Wnt/ß-catenin signaling and metabolic disorders as well as the inhibitory effects of SFRP1 on this signaling pathway, the present work aimed to investigate the correlation between serum SFRP1 levels and type 2 diabetes mellitus (T2DM) and its developing risk factors for the first time. METHODS: This case-control study measured serum levels of SFRP1, tumor necrosis factor (TNF)-α, interleukin (IL)-6, adiponectin, and fasting insulin using enzyme-linked immunosorbent assay kits in 80 T2DM patients and 80 healthy individuals. Biochemical parameters were determined using the AutoAnalyzer instrument. RESULTS: The T2DM group had higher levels of SFRP1 compared with the controls (146.8100 ± 43.61416 vs 81.9531 ± 32.78545 pg/mL; P < .001). There was a positive correlation between SFRP1 and insulin (r = 0.327, P = .003), TNF-α (r = 0.420, P < .001) as well as homeostatic model assessment for insulin resistance (r = 0.328, P = .003) in the T2DM group. In addition, 10-unit changes in SFRP1 levels showed the risk of T2DM in both the unadjusted (odds ratio [OR] [95% CI] = 1.564 [1.359-1.800]) and adjusted models accounting for age, gender, and body mass index (OR [95% CI] = 1.564 [1.361-1.799]; P < .001). A cut-off value of SFRP1 (105.83 pg/mL) was identified to distinguish between the T2DM patients and the healthy subjects, with sensitivity of 75.0% and specificity of 80.0%. CONCLUSION: According to our research, there was a significant and positive link between the amount of SFRP1 and the likelihood of developing T2DM as well as the related factors like insulin resistance index and TNF-α. These results indicated that SFRP1 might have a potential role in the development of T2DM.

Role of Fibrinogen-like Protein 1 in Tumor Recurrence Following Hepatectomy.

Partial hepatectomy is a first-line treatment for hepatocellular carcinoma. Within 2 weeks following partial hepatectomy, specific molecular pathways are activated to promote liver regeneration. Nevertheless, residual microtumors may also exploit these pathways to reappear and metastasize. Therapeutically targeting molecules that are differentially regulated between normal cells and malignancies, such as fibrinogen-like protein 1 (FGL1), appears to be an effective approach. The potential functions of FGL1 in both regenerative and malignant cells are discussed within the ambit of this review. While FGL1 is normally elevated in regenerative hepatocytes, it is normally downregulated in malignant cells. Hepatectomy does indeed upregulate FGL1 by increasing the release of transcription factors that promote FGL1, including HNF-1α and STAT3, and inflammatory effectors, such as TGF-ß and IL6. This, in turn, stimulates certain proliferative pathways, including EGFR/Src/ERK. Hepatectomy alters the phase transition of highly differentiated hepatocytes from G0 to G1, thereby transforming susceptible cells into cancerous ones. Activation of the PI3K/Akt/mTOR pathway by FGL1 allele loss on chromosome 8, a tumor suppressor area, may also cause hepatocellular carcinoma. Interestingly, FGL1 is specifically expressed in the liver via HNF-1α histone acetylase activity, which triggers lipid metabolic reprogramming in malignancies. FGL1 might also be involved in other carcinogenesis processes such as hypoxia, epithelial-mesenchymal transition, immunosuppression, and sorafenib-mediated drug resistance. This study highlights a research gap in these disciplines and the necessity for additional research on FGL1 function in the described processes.

CCN3/NOV serum levels in coronary artery disease (CAD) patients and its correlation with TNF-α and IL-6.

INTRODUCTION: Dysregulation in the secretion of adipokines or adipocytokines plays a significant role in triggering a pro-inflammatory state, leading to endothelial dysfunction and insulin resistance, and ultimately elevating the risk of atherosclerosis and coronary artery disease (CAD). Previous studies have shown a link between NOV/CCN3 (an adipokine) and obesity, insulin resistance, and inflammation. However, no research has explored the relationship between CCN3 serum levels and CAD. Therefore, we conducted the first investigation to examine the correlation between CCN3 and CAD risk factors in patients. METHODS: In a case-control study, we measured the serum levels of CCN3, IL-6, adiponectin, and TNF-α in 88 angiography-confirmed CAD patients and 88 control individuals using ELISA kits. Additionally, we used an auto analyzer and commercial kits to measure the biochemical parameters. RESULTS: In patients with CAD, the serum levels of CCN3, TNF-α, and IL-6 were significantly higher compared to the control group, whereas lower levels of adiponectin were observed in the CAD group (P < 0.0001). A positive correlation was found between CCN3 and IL-6 and TNF-α in the CAD group ([r = 0.38, P < 0.0001], [r = 0.39, P < 0.0001], respectively). A binary logistic regression analysis showed the risk of CAD in the model adjusted (OR [95% CI] = 1.29 [1.19 - 1.41]), (P < 0.0001). We determined a cut-off value of CCN3 (3169.6 pg/mL) to distinguish CAD patients from the control group, with good sensitivity and specificity obtained for this finding (83.8% and 87.5%, respectively). CONCLUSION: This study provides evidence of a positive association between CCN3 serum levels and CAD, as well as inflammation markers such as IL-6 and TNF-α. These findings suggest that CCN3 may serve as a potential biomarker for CAD, and further investigations are necessary to validate this association and explore its potential use in clinical settings.

A positive association of serum CCN5/WISP2 levels with the risk of developing gestational diabetes mellitus: a case-control study.

INTRODUCTION: CCN5/WISP2 is prominently manifest in adipose tissue and has been linked to the pathogenesis of obesity, diabetes, and insulin resistance. However, discrepancies exist in previous studies, and little is known about its association with gestational diabetes mellitus (GDM). The current investigation is designed to examine the correlation of WISP2 with risk factors in GDM patients in comparison to healthy pregnant women for the first time. METHODS: This case-control study measured serum levels of CCN5, TNF-α, IL-6, adiponectin, and fasting insulin using ELISA kits in 88 GDM patients and 88 pregnant women. RESULTS: The GDM group had remarkably higher serum levels of CCN5 (379.41 ± 83.078 ng/ml) compared to controls (212.02 ± 77.935 ng/ml). In a similar vein, it was observed that patients diagnosed with GDM exhibited elevated levels of pro-inflammatory cytokines such as IL-6 and TNF-α; while conversely, adiponectin levels were found to be significantly lower than those observed in the control group (P < 0.0001). In women with GDM, a positive and significant correlation was observed between CCN5 and BMI, FBG, insulin, HOMA-IR, as well as IL-6 and TNF-α levels. In the adjusted model, the risk of GDM was significantly increased with elevated serum CCN5 level. CONCLUSION: Our research indicates a noteworthy and affirmative correlation between the levels of CCN5 in the serum and the risk of developing GDM, along with its associated risk factors such as BMI, insulin resistance index, FBG, and inflammatory cytokines (TNF-α and IL-6). These findings suggest that CCN5 could potentially play a role in the etiology of GDM.

The effects of probiotic and synbiotic supplementation on inflammation, oxidative stress, and circulating adiponectin and leptin concentration in subjects with prediabetes and type 2 diabetes mellitus: a GRADE-assessed systematic review, meta-analysis, and meta-regression of randomized clinical trials.

PURPOSE: Probiotics or synbiotics consumption have been suggested to reduce the risk of cardiovascular disease (CVD) through a decline in inflammation and oxidative stress, however, the results from studies are conflicting. This study filled this knowledge gap by evaluating randomized controlled trials (RCTs) investigating probiotics or synbiotics intake on adipokines, inflammation, and oxidative stress in patients with prediabetes and type-2 diabetes mellitus (T2DM). METHODS: We systematically did search up to March 2022 in PubMed/Medline, Scopus, ISI Web of Science, and Cochrane library. A random-effect model was applied to estimate the weighted mean difference (WMD) and 95% confidence interval (95% CI) for each outcome. RESULTS: A total of 32 RCTs were included in the meta-analysis. This intervention led to a significant decrease in levels of C-reactive protein (CRP) (WMD - 0.62 mg/l; 95% CI - 0.80, - 0.44; p < 0.001), tumor necrosis factor-α (TNF-α) (WMD - 0.27 pg/ml; 95% CI - 0.44, - 0.10; p = 0.002) and malondialdehyde (MDA) (WMD - 0.51 µmol/l; 95% CI - 0.73, - 0.30; p < 0.001), and also a significant increase in levels of glutathione (GSH) (WMD 69.80 µmol/l; 95% CI 33.65, 105.95; p < 0.001), total antioxidant capacity (TAC) (WMD 73.59 mmol/l; 95% CI 33.24, 113.95; p < 0.001) and nitric oxide (NO) (WMD 7.49 µmol/l; 95% CI 3.12, 11.86; p = 0.001), without significant alterations in interleukin-6 (IL-6) and adipokines levels. CONCLUSION: A consumption of probiotics or synbiotics could be a useful intervention to improve cardiometabolic outcomes through a reduced inflammation and oxidative stress in patients with prediabetes and T2DM.

Ameliorative impacts of polymeric and metallic nanoparticles on cisplatin-induced nephrotoxicity: a 2011-2022 review.

Cisplatin (CDDP) is a well-known platinum-based drug used in the treatment of various malignancies. However, the widespread side effects that this drug leaves on normal tissues make its use limited. Since cisplatin is mainly eliminated from the kidneys, CDDP-induced nephrotoxicity is the most significant dose-limiting complication attributed to cisplatin, which often leads to dose withdrawal. Considering the high efficiency of cisplatin in chemotherapy, finding renoprotective drug delivery systems for this drug is a necessity. In this regard, we can take advantages of different nanoparticle-based approaches to deliver cisplatin into tumors either using passive targeting or using specific receptors. In an effort to find more effective cisplatin-based nano-drugs with less nephrotoxic effect, the current 2011-2022 review study was conducted to investigate some of the nanotechnology-based methods that have successfully been able to mitigate CDDP-induced nephrotoxicity. Accordingly, although cisplatin can cause renal failures through inducing mitochondria dysfunction, oxidative stress, lipid peroxidation and endoplasmic reticulum stress, some CDDP-based nano-carriers have been able to reverse a wide range of these advert effects. Based on the obtained results, it was found that the use of different metallic and polymeric nanoparticles can help renal cells to strengthen their antioxidant systems and stay alive through reducing CDDP-induced ROS generation, inhibiting apoptosis-related pathways and maintaining the integrity of the mitochondrial membrane. For example, nanocurcumin could inhibit oxidative stress and acting as a ROS scavenger. CONPs could reduce lipid peroxidation and pro-inflammatory cytokines. CDDP-loaded silver nanoparticles (AgNPs) could inhibit mitochondria-mediated apoptosis. In addition, tea polyphenol-functionalized SeNPs (Se@TE) NPs could mitigate the increased level of dephosphorylated AKT, phosphorylated p38 MAPK and phosphorylated c-Jun N-terminal kinase (JNK) induced by cisplatin. Moreover, exosomes mitigated cisplatin-induced renal damage through inhibiting Bcl2 and increasing Bim, Bid, Bax, cleaved caspase-9, and cleaved caspase-3. Hence, nanoparticle-based techniques are promising drug delivery systems for cisplatin so that some of them, such as lipoplatins and nanocurcumins, have even reached phases 1-3 trials.

Renal, cardiac, neurological, cutaneous and coagulopathic long-term manifestations of COVID-19 after recovery; A review.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) caused the novel global coronavirus disease 2019 (COVID-19) disease outbreak. Its pathogenesis is mostly located in the respiratory tract. However, other organs are also affected. Hence, realising how such a complex disturbance affects patients after recovery is crucial. Regarding the significance of control of COVID-19-related complications after recovery, the current study was designed to review the cellular and molecular mechanisms linking COVID-19 to significant long-term signs including renal and cardiac complications, cutaneous and neurological manifestations, as well as blood coagulation disorders. This virus can directly influence on the cells through Angiotensin converting enzyme 2 (ACE-2) to induce cytokine storm. Acute release of Interleukin-1 (IL1), IL6 and plasminogen activator inhibitor 1 (PAI-1) have been related to elevating risk of heart failure. Also, inflammatory cytokines like IL-8 and Tumour necrosis factor-α cause the secretion of von Willebrand factor (VWF) from human endothelial cells and then VWF binds to Neutrophil extracellular traps to induce thrombosis. On the other hand, the virus can damage the blood-brain barrier by increasing its permeability and subsequently enters into the central nervous system and the systemic circulation. Furthermore, SARS-induced ACE2-deficiency decreases [des-Arg9]-bradykinin (desArg9-BK) degradation in kidneys to induce inflammation, thrombotic problems, fibrosis and necrosis. Notably, the angiotensin II-angiotensin II type 1 receptor binding causes an increase in aldosterone and mineralocorticoid receptors on the surface of dendritic cells cells, leading to recalling macrophage and monocyte into inflammatory sites of skin. In conclusions, all the pathways play a key role in the pathogenesis of these disturbances. Nevertheless, more investigations are necessary to determine more pathogenetic mechanisms of the virus.

Effects of Folic Acid Supplementation on Inflammatory Markers: A Grade-Assessed Systematic Review and Dose-Response Meta-Analysis of Randomized Controlled Trials.

It has been theorized that folic acid supplementation improves inflammation. However, its proven effects on inflammatory markers are unclear as clinical studies on this topic have produced inconsistent results. To bridge this knowledge gap, this systematic review and meta-analysis of randomized controlled trials (RCTs) aimed to evaluate the effects of folic acid supplementation on serum concentrations of the inflammatory markers C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Methods: To identify eligible RCTs, a systematic search up to April 2021 was completed in PubMed/Medline, Scopus, Web of Science, EMBASE, Cochrane databases, and Google Scholar using relevant keywords. A fix or random-effects model was utilized to estimate the weighted mean difference (WMD) and 95% confidence interval (95% CI). Results: Twelve RCTs were included in the present meta-analysis. The pooled analysis revealed that serum concentrations of CRP (WMD: -0.59 mg/L, 95% CI -0.85 to -0.33, p < 0.001) were significantly reduced following folic acid supplementation compared to placebo, but did not affect serum concentrations of IL-6 (WMD: -0.12, 95% CI -0.95 to 0.72 pg/mL, p = 0.780) or TNF-α (WMD: -0.18, 95% CI -0.86 to 0.49 pg/mL, p = 0.594). The dose-response analysis demonstrated a significant relationship between an elevated dosage of folic acid supplementation and lower CRP concentrations (p = 0.002). Conclusions: We found that folic acid supplementation may improve inflammation by attenuating serum concentrations of CRP but without significant effects on IL-6 and TNF-α. Future RCTs including a larger number of participants and more diverse populations are needed to confirm and expand our findings.

The Shift of HbF to HbA under Influence of SKA2 Gene; A Possible Link between Cortisol and Hematopoietic Maturation in Term and Preterm Newborns.

BACKGROUND: We hypothesized that the SKA2 gene can convert hemoglobin F to A leading to the maturity of the hematopoietic system by glucocorticoid hormone; so, the present study aimed to investigate the health outcome of newborns by using the effect of SKA2 gene on hematopoietic maturation. METHODS: At first, 142 samples were divided into term and preterm. After sampling from the umbilical cord blood, the expression of SKA2 genes and HbA and F were evaluated by quantitative RT-PCR. The blood gases were measured by Campact 3 device. Finally, the cortisol level was measured by ELISA method and HbA and F levels were investigated by capillary electrophoresis. RESULTS: The blood gases and Apgar scores were more favorable in term newborns (P <0.001). Levels of protein/expression of HbF in newborns with Apgar score greater than 7 was lower than that of the newborns with Apgar score below 7 (P <0.001). Cortisol and HbA levels were considerably higher in term newborns compared to the preterm ones (P <0.001). In the preterm and term groups, SKA2 gene expression had a positive and significant relationship with cortisol and HbA levels as well as a negative relationship with the HbF level. In the preterm group, a positive and significant relationship was observed between the expression of SKA2 and HbF genes. CONCLUSION: The results revealed that the SKA2 gene affected hematopoietic maturation in preterm and term newborns and the health outcome of newborns improved by increasing HbA level.

Anti-Inflammatory Effects of Plasma Circulating Exosomes Obtained from Normal-Weight and Obese Subjects on Hepatocytes.

INTRODUCTION: Obesity is a disorder with low-grade chronic inflammation that plays a key role in hepatic inflammation and steatosis. Moreover, there are studies to support the role of exosomes in cellular communications, the regulation of metabolic homeostasis and immunomodulatory activity. Accordingly, we aimed to evaluate the influence of plasma circulating exosomes derived from females with normal-weight and obesity on the secretion of inflammatory cytokines in human liver cells. METHODS: Plasma circulating exosomes were isolated from four normal (N-Exo) and four obese (OExo) women. The exosomes were characterized and approved for CD63 expression (common exosomal protein marker) and morphology/size using the western blot and TEM methods, respectively. The exosomes were used for the stimulation of HepG2 cells in vitro. After 24 h of incubation, the protein levels of TNF-α, IL-6, and IL-1ß were measured in the culture supernatant of HepG2 cells using the ELISA kit. RESULTS: The protein levels of IL-6 and TNF-α in the cells treated with O-Exo and N-Exo reduced significantly in comparison with the control group (P=0.039 and P<0.001 respectively), while significant differences were not found between normal and obese groups (P=0.808, and P=0.978 respectively). However, no significant differences were found among the three groups in terms of IL-1ß levels (P=0.069). Based on the correlation analysis, the protein levels of IL-6 were positively correlated with TNF-α (r 0.978, P<0.001). CONCLUSION: These findings suggest that plasma circulating exosomes have probably antiinflammatory properties independent of body mass index and may decrease the secretion of inflammatory cytokines in the liver. However, further in vitro and in vivo investigations are needed to address the anti-inflammatory function of N-Exo and O-Exo in human liver cells and/or other cells.

Influence of plasma circulating exosomes obtained from obese women on tumorigenesis and tamoxifen resistance in MCF-7 cells.

Obesity is associated with breast cancer aggressiveness and drug resistance. Although the underlying mechanisms are unknown, recent studies indicated that exosomes have a principal contributory role in obesity-associated metabolic complications. Hence, we investigated whether obesity can mediate breast cancer progression and resistance to tamoxifen by plasma-derived-exosomes from obese women or not. Plasma exosomes isolated from five normal-weight (N-Exo) and five obese women (O-Exo) were characterized for size, zeta potential, and CD63 expression. After the treatment of MCF-7 cells with N-Exo and O-Exo, cell proliferation, migration, invasion as well as levels of MMP-9 and MMP-2 were evaluated by the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, wound healing, transwell, and zymography methods, respectively. For evaluating resistance to tamoxifen, the cell viability, apoptosis, and the p53 protein were evaluated using the MTT assay, flow cytometry, and western blot methods, respectively. Cell proliferation, migration, and invasion were significantly increased in the cells treated with O-Exo than untreated cells (p = .001, p = .018, p = .034, respectively). Levels of MMP-2 and MMP-9 were remarkably increased in the cells treated with O-Exo in comparison with ones treated with N-Exo (p = .040, p = .043, respectively). As for resistance to tamoxifen, O-Exo had significantly the greater anti-apoptotic effects in comparison with the N-Exo group (p = .013). Besides, p53 levels were significantly decreased in the cells treated with O-Exo than ones treated with N-Exo (p = .045). The cell viability was significantly more in cells treated with O-Exo in comparison with the cells only treated with tamoxifen (p = .040). Our findings demonstrated that circulating exosomes derived from obese women could lead to tumorigenesis and tamoxifen resistance in breast cancer cells. However, more studies are needed to establish this notion.

Serum C1q/TNF-Related Protein-2 (CTRP2) Levels are Associated with Coronary Artery Disease.

Recent studies have shown that complement C1q tumor necrosis factor related proteins (CTRPs) such as adiponectin, have different regulatory roles on the cardiovascular system. CTRP2 is the most similar to adiponectin and one of the best characterized beneficial adipokines important in the regulation of whole body metabolism. However, there were no studies about the relationship between CTRP2 and Coronary artery disease (CAD). This study aimed to evaluate the serum CTRP2 levels in patient with Coronary artery disease. In this study, a total of 82 participants who underwent vascular angiography were included. All of subjects were male. According to their coronary angiography results, all participants were divided into CAD group (n = 42) and control group (n = 40). Serum CTRP2 levels were determined quantitatively with enzyme-linked immunosorbent assay (ELISA). Our study for the first time showed that the CTRP2 levels were higher in CAD patients (1.79 ± 1.46 ng/mL) compared to control subjects (1.08 ± 0.78 ng/mL; p = 0.001). The levels of CTRP2 also were positively correlated with severity of CAD (r = 0.356, p = 0.001). In addition, logistic regression analysis indicated that CTRP2 had an independent association with the risk of CAD (OR [CI] = 3.366 [1.605-7.060]; p = 0.001). Increased levels of CTRP2 in CAD patients were independently associated with the progression of the CAD, it might be regarded as a novel biomarker for assessing the risk of CAD; however, more study is required in this regard.

Association of GRP78, HIF-1α and BAG3 Expression with the Severity of Chronic Lymphocytic Leukemia.

INTRODUCTION: Parallel with the progression of Chronic Lymphocytic Leukemia (CLL), the levels of 78KDa Glucose-Regulated Protein (GRP78) and Hypoxia-Inducible Factor 1 alpha (HIF-1α) are increased as they may activate the induction of anti-apoptotic proteins such as BCL2 Associated Athanogene 3 (BAG3). Previous studies have indicated that there is a positive correlation among GRP78, HIF-1α and BAG3. OBJECTIVE: This study aimed to evaluate the effect of metabolic factors involved in invasive CLL on apoptotic factors. METHODS: A case-control study was conducted on 77 patients diagnosed with CLL along with 100 healthy individuals. Cell blood count was performed for all participants. According to Binet's classification, CLL patients were divided into different groups. B cells were isolated from the peripheral blood of CLL patients by binding to anti-CD19 beads. The expression of BAG3, GRP78 and HIF-1α genes was analyzed using the RT-PCR method. To confirm the results of RT-PCR, western blot analysis was carried out. RESULTS: The results showed that there was a strong association among the expression of BAG3, GRP78 and HIF-1α. The stage of CLL in patients was highly correlated with the expression rate of each gene (p<0.001). Accordingly, the western blot analysis indicated that the concentrations of GRP78 and HIF-1α were significantly higher than the expression of BAG3, considering the stage of CLL. CONCLUSION: It was shown that increased expression of GRP78 and HIF-1α could result in the elevation of BAG3, as well as the disease progression. Therefore, the role of these metabolic factors might be more pronounced compared with the anti-apoptotic agents to monitor disease progression in CLL patients.

The Influence of Psychological Stress on the Initiation and Progression of Diabetes and Cancer.

CONTEXT: Psychological stress can be considered a risk factor for the initiation and progression of many pathological conditions, including type 1 and 2 diabetes mellitus and cancer. OBJECTIVES: The aim of this review article was to evaluate the molecular and cellular mechanisms linking psychological stress to the onset and progression of diabetes and cancer. EVIDENCE ACQUISITION: The current review was conducted to survey and analyze studies related to the effects of psychological stress on diabetes and cancer. RESULTS: Psychological stress may make individuals prone to the development of diabetes through the impairment of the hypothalamic-pituitary-adrenal (HPA) axis function, sympathetic nerves system (SNS), lipid profile, cytokines balance, renin-angiotensin system (RAS), and insulin signaling pathway. Additionally, psychological stress can contribute to the development of cancer through the perturbation in the HPA axis, SNS function, and cytokines balance. Psychological stress is also capable of decreasing the levels of oxytocin and dopamine, leading to an increased risk of cancer in susceptible individuals. CONCLUSIONS: It seems that psychological stress plays a significant role in the onset and progression of diabetes and cancer. The identification of the pathways triggered by psychological stress would open up a new avenue for the understanding of molecular mechanisms by which diabetes and cancer could be managed or even prevented.

The Effect of Hydro-Alcoholic Extract of Foeniculum vulgare Mill on Leukocytes and Hematological Tests in Male Rats.

BACKGROUND: Medicinal plants have a long history in treating blood disorders, which is one of the most common problems in today's advanced world. Fennel (Foeniculum vulgare) is a medicinal plant with a high content of polyphenols and has antioxidant and immunomodulatory properties. OBJECTIVES: The aim of this study was to evaluate the effect of hydro-alcoholic extract of fennel on some hematological indices in male rats. MATERIALS AND METHODS: In this experimental study, thirty male Wistar rats were divided into six groups (five rats in each group). The first group (control) did not receive any dose; the second group (sham) received 1 mL normal saline (extraction solvent); and the experimental groups 1, 2, 3 and 4 respectively received 1 mL hydro alcoholic extract of fennel in four doses of 250, 500, 750 and 1000 mg/kg of body weight every 48 hours for 30 days by gavage. One day after the last gavage following induction of anesthesia and taking blood from the heart of rats, measurement of red and white blood cells, hemoglobin, hematocrit and tests of bleeding and coagulation time (CT) were performed. The data was analyzed by one-way ANOVA test using SPSS15 software. RESULTS: Fennel increased mean RBC (7.54 ± 0.53 × 106) and WBC (5.89 ± 0.78 × 103) values, especially at a dose of 250 mg/mL and CT (2.45 ± 0.20) at a dose of 500mg/mL compared to the control group (P < 0.05). CONCLUSIONS: Fennel increased red and white blood cells probably due to the presence of polyphenols and antioxidant activity of fennel and reduced negative effects of free radicals on blood cells.