Objective: To investigate the anti-hyperlipidemic, anti-inflammatory and analgesic properties of of E. longifolia root extract in animal models. Methods:In this study, glucose-fructose enriched diet-induced hyperlipidemia, carrageenan-induced paw edema and acetic acid-induced writhing were used to evaluate the anti-hypertriglyceridemia, anti-inflammatory and analgesic activities, respectively. At the end of the experiment of glucose-fructose enriched diet-induced hyperlipidemia, blood samples were collected and estimation of blood lipids were carried out. Edema thickness was measured using digital caliper at 0, 15, 30, 45, 60, 90, 120, 150, 180, 210, 240, 270, 300, 330, and 360 min after carrageenan injection. The number of abdominal writhing for each mouse was observed and counted during a period of 1 h post injection of acetic acid.Results: E. longifolia root extract demonstrated a significant reduction of triglyceride levels (p<0.05) compared with the control group in glucosefructose enrich diet in rats. In anti-inflammatory test, the extract significantly inhibited the carrageenan induced paw edema formation (p<0.05). The extract also significantly decreased the number of writhing in acetic acid-induced mice (p<0.05).Conclusion: E. longifolia root extract shown a significant anti-hypertriglyceridemia, anti-inflammatory and analgesic activities. Further studies are needed to determine mechanisms for its acitivities of E. longifolia root extract.
Nicotine, the active compound in cigarettes, was considered as the risk factor for type 2 diabetes mellitus (T2DM). In the human body, nicotine would be metabolized by the enzyme cytochrome P450 2A6 (CYP2A6). CYP2A6 was known to be highly polymorphic. The active form of this gene was CYP2A6 *1, while the CYP2A6 *4 and CYP2A *9 alleles were the inactive alleles. The presence of this inactive allele caused the decreased activity of CYP2A6 so that it would affect the level of nicotine in the blood and would eventually cause an increased blood sugar levels. This study aimed to determine the effect of CYP2A6 polymorphism on glycohemoglobine levels among Javanese smokers. The blood sugar levels were measured by hemoglobin A1c (HbA1c). In this study, 33 active smokers involved in the study were identified as slow metabolizers, by which 63.9% of all test participants had CYP2A6 *1/*4 genotype and as many as 6.1% of the test participants had the CYP2A6 *1/*4/*9. The HbA1c levels among the participants have been analyzed, 28 participants were in normal range (4.83-5.56%); 4 participants were identified in prediabetes condition (5.70%-5.97%) and 1 participant was in diabetes with HbA1c level was 7.16%. This condition indicates that the presence of CYP2A6 *4 and *9 alleles will affect HbA1c levels which can eventually lead to T2DM disease.
Purpose This study aimed to explore the association of rs857148 A>C as 3ʹUTR variants with blood pressure, HbA1c profile, and lipid profiles as cardiometabolic parameters among patients with T2DM receiving metformin. Patients and Methods This cross-sectional analytic research was conducted with 114 consecutively selected patients with T2DM. Polymerase chain reaction-restriction fragment length polymorphism was conducted to determine rs857148 . A total of 108 patients fulfilled inclusion and exclusion criteria. Results Genotype distribution agreed with the Hardy Weinberg Equation for Equilibrium ( p >0.05) but wildtype allele was found as the minor allele. Subjects with CC genotype and C allele had enhanced HbA1c levels (OR=7.12; 95% CI=1.05–48.26; p =0.04; OR=1.66; 95% CI=1.06–2.60; p =0.03, respectively). It was confirmed by dominant model whereas subjects with AA tended to have reduced HbA1c compared to AC+CC genotype (OR=0.15; 95% CI=0.02–0.97; p =0.047). AC genotype had significant correlation to total cholesterol (OR=1.05; 95% CI=1.01–1.10; p =0.03) compared to AA genotype. Conclusion We conclude that polymorphism of rs87148 , specifically CC genotype and C allele, has a significant association with HbA1c and total cholesterol after considering oral hypoglycemia agent dose, age, gender, and combination therapy, compared to AA genotype. Future studies that involve a larger sample population and more rigorous selection criteria are required.
Infarction stroke is a leading cause mortality and disability in the world. Appropriate management of acute infarction stroke will be able to reduced morbidity and mortality of the disease. Many laboratory parameters which can be done for detecting risk of prognosticfactors, one of them is serum uric acid concentration. The aim of this study is to know if hyperuricemia is prognostic factor for clinicaloutcome in acute infarction stroke.A prospective cohort study was carried out, compare between two groups of exposed and non-exposedgroup. Subjects who meet inclusion and exclusion criteria was involved in the study. The exposed group was a group of acute infarctionstroke patients who exposed to hyperuricemia, in other hand, patient who do not have hyperuricemia was separated as the non-exposedgroup. Inception cohort was applied when patient admits to emergency unit during 48 hours of onset, age ≥ 40 years old, man orwoman, have signed informed consent are inclusion criteria. Gadjah Mada Stroke Scale and serum uric acid concentration was measured on admission. Patient with haemorhage stroke and who are taking medicine that cause decrease uric acid are excluded. Test of serum uric acid concentration was performed by using Vitros 250, dry chemistry system. Patients were followed up 7 days in Neurology Unitand the outcome were measured by evaluating a score of Gadjah Mada Stroke Scale. Prognostic factor hyperuricemia has RR= 2.159(95% CI: 0.684-6.816), p= 0.158 for outcome. Hyperuricemia is not be evident as prognostic factor in acute infarction stroke.
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