Rats' umbilical-cord mesenchymal stem cells ameliorate mast cells and Hsp70 on ovalbumin-induced allergic rhinitis rats.

Aim Allergic rhinitis (AR) is a heterogeneous condition that has been associated with inflammatory responses and is characterized by clinical typical symptoms of nasal itching, sneezing, watery discharge and congestion. Mesenchymal stem cells (MSCs) are multipotent stem cells that have the immunoregulatory ability by secreting various cytokines which potent as a promising therapeutic modality for allergic airway diseases, including AR. The aim of this study was to investigate the effect of rat UC-MSCs on the number of mast cells, the expression of Hsp70 indicated by the nasal symptoms allergic, particularly nasal rubbing in ovalbumininduced AR rats. Methods Fifteen male Wistar rats (6 to 8 weeks old) were randomly divided into three groups (control group, sham group, and OVA+MSCs group). OVA nasal challenge was conducted daily from day 15 to 21, and UC-MSCs (1x106 ) were administrated intraperitoneally to OVA-sensitized rats on day 21. Nasal rubbing was observed from day 22 to 28. The rats were sacrificed on day 22 and day 28. The nasal cavity tissues were prepared for histological observations. Results The administration of UC-MSCs could reduce the number of mast cells and the expression of Hsp70 leading to reduction of nasal symptoms allergic, particularly nasal rubbing. Conclusion Based on this finding, MSCs present a promising immediate curative effect to the inflammatory reaction in AR rats.

Anti-fibrotic effect of intravenous umbilical cord-derived mesenchymal stem cells (UC-MSCs) injection in experimental rats induced liver fibrosis.

Aim To investigate the effect of umbilical cord-derived mesenchymal stem cells (UC-MSCs) administration among liver fibrosis experimental rat model via the regulation of angiotensin II type 1 receptor (AT1R) and platelet-derived growth factor-ß (PDGF-ß) due to their therapeutic potential to replace liver transplantation for advanced liver fibrosis. Yet the mechanism of action has been questionably associated with UC-MSCs fibrosis regression properties. Methods Sprague-Dawley (SD) rats (n=18) were separated into three groups (control, untreated liver fibrosis, and UC-MSCs treated group). Serum PDGF-ß level was determined by enzymelinked immunosorbent assay (ELISA) following 14 days of UCMSCs injection. Meanwhile, AT1R expression was interpreted based on immunoreactive score (IRS) stained using polyclonal antibody and liver fibrosis stained with hematoxylin & eosin was graded using the METAVIR score. Results UC-MSCs were isolated successfully from rat umbilical cord. Liver fibrosis was observed following 14 weeks of CCl4 injection concurrent with higher serum level of PDGF-ß, but the UC-MSCs-treated group had lower level (980.08 ±289.41 and 606.42±109.85 for untreated liver fibrosis and UC-MSCs treated group, respectively; p=0.004). There was also a high expression of AT1R among untreated liver fibrosis group, as well as highgrade liver fibrosis versus localized fibrosis and low level of AT1R expression among UC-MSCs treated-group (p=0.001). Conclusion UC-MSCs administration could ameliorate liver fibrosis by reducing the AT1R expression and PDGF-ß serum levels, and intervention through this signaling pathway could be alternative evidence for the causative of positive outcome.

Combination of vitamin A and D supplementation for ischemic stroke: effects on interleukin-1ß and clinical outcome.

Aim Accumulated evidence suggests that vitamin A and D agonists can alleviate the development of atherosclerosis. Therefore, the aim of this study was to determine the effect of vitamin A and D combination supplement on interleukin-1ß (IL-1ß) and clinical outcome in ischemic stroke. Methods A single-blind, randomized controlled trial was conducted on ischemic stroke patients at Adam Malik Hospital between March 2018 to February 2019. The patients were randomized into 4 groups of the treatment consisting of supplementation using vitamin A or D only, combination of vitamin A and D, and placebo group, all given for 12 weeks. Clinical outcome was determined using the National Institute of Health Stroke Scale (NIHSS). At the time of admission and after the treatment was completed, all patients were measured for vitamin A, vitamin D, and IL-1ß serum level, and NIHSS score. Results From the total of 120 patients, in the combination group there were significant increments on both vitamin A (p=0.04) and vitamin D (p=0.01) serum level after 12 weeks of the treatment, compared to the other groups. In conjunction, IL-1ß serum level showed a significant decrement in the combination group (p<0.001). Lastly, the biggest improvement of NIHSS could be seen in the combination group, which was marked by the highest decrement of NIHSS score (p<0.001). Conclusion Administration of combination of vitamin A and D supplementation can significantly increase vitamin A and D serum level, decrease IL-1ß serum level, and ultimately improve clinical outcome in ischemic stroke patients.

Is there an association between alpha 2-Heremans-Schmid glycoprotein (AHSG) gene Thr256Ser polymorphisms with aortic calcification in regular hemodialysis patients in Medan, Indonesia.

Aim Alpha2-Heremans-Schmid glycoprotein (AHSG), a circulating plasma protein, plays an essential role in bone and vascular mineralization. The impact of AHSG gene polymorphisms on aortic calcification in haemodialysis patients was inconsistent. We performed this study to clarify precise association among AHSG gene Thr256Ser single-nucleotide polymorphisms and aortic calcification. Methods Patients on stable regular haemodialysis treatment for more than thirty months were included in a cross-sectional study at Rasyida Renal Hospital Medan. Lateral spine X-rays were performed to evaluate the aortic calcification. Genotyping for the polymorphisms was carried out using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) techniques. Results Aortic calcification was detected in 69.8% of patients. From 106 patients, 49 patients (46.2 %) had CC (Thr/Thr), 54 (51.0%) had CG (Thr/Ser) and three (2.8%) patients had GG (Ser/ Ser) polymorphism. The proportion of patients with heterozygous or homozygous G allele (CG and GG genotypes) is more likely (91.2%) to have aortic calcification. The bivariate analysis showed that Thr256Ser polymorphism (G allele) was associated with increased risk for aortic calcification (PR=2.03; 95% CI 1.48-2.80; p<0.001). However, overall results from multivariate analysis showed that Fetuin-A level <204 pg/mL (PR=22.0; 95% CI 3.32-145.91; p=0.001) and IL-6 level ≥53.05 mg/dL (PR=19.50; 95% CI 2.87-132.41; p=0.002) were the major risk factors for the occurrence of aortic calcification. Conclusion AHSG Thr256Ser gene polymorphism showed an association with aortic calcification in regular haemodialysis patients, but Fetuin-A and IL-6 have a dominant role in the development of aortic calcification.

Effect of Flunarizine on Serum Glutamate Levels and its Correlation with Headache Intensity in Chronic Tension-Type Headache Patients.

BACKGROUND: Some of the excitatory neurotransmitters including glutamate have been suggested to be involved in headache pathophysiology. To our knowledge, there is a lack of publication about flunarizine efficacy in chronic tension-type headache (CTTH) treatments and the roles of glutamate in CTTH pathophysiology. AIM: This study aimed to investigate the flunarizine effect on serum levels of glutamate and its correlation with headache intensity based on the Numeric Rating Scale for pain (NRS) scores in CTTH patients. METHOD: In a prospective randomised, double-blind study with pre and post-test design, seventy-three CTTH patients were randomly allocated with flunarizine 5 mg, flunarizine 10 mg and amitriptyline 12.5 mg groups. The serum levels of glutamate and NRS scores were measured before and after 15-day treatment. RESULTS: Flunarizine 5 mg was more effective than flunarizine 10 mg and amitriptyline 12.5 mg in reducing serum glutamate levels, whereas amitriptyline 12.5 mg was the most effective in reducing headache intensity. There was found nonsignificant, but very weak negative correlation between headache intensity and serum glutamate levels after flunarizine 5 mg administration (r = -0.062; P = 0.385), nonsignificant very weak negative correlation after flunarizine 10 mg administration (r = -0.007; P = 0.488) and there was found a significant moderate positive correlation (r = 0.508; P = 0.007) between headache intensity and serum glutamate levels after amitriptyline 12.5 mg administration. CONCLUSION: Since there was no significant correlation found between serum glutamate and headache intensity after treatment with flunarizine, it is suggested that decreasing of headache intensity after flunarizine treatment occurred not through glutamate pathways in CTTH patients.