Syahrijuita Kadir
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Simvastatin Toxicity Induces Mitochondrial Dysfunction in Rat Skeletal Muscle Zulfahmidah; Marhaen Hardjo; Syahrijuita Kadir
Indian Journal of Forensic Medicine & Toxicology Vol. 15 No. 3 (2021): Indian Journal of Forensic Medicine & Toxicology
Publisher : Institute of Medico-legal Publications Pvt Ltd

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37506/ijfmt.v15i3.16023

Abstract

Background: Statins are the class of drugs that are widely used for lowering LDL cholesterol and as primary and secondary prevention to cardiovascular disease. However, the widespread use of statins is constrained by the presence of toxicity or intolerance, which affects drug control rates. The toxicity or intolerance of statins ranges from 10-15%. The most common statin toxicity is statin-associated muscle symptoms (SAMS). The underlying mechanisms of SAMS involve the disruption of mitochondrial biogenesis, potential membrane changes, reduced number of mitochondria, and changes in protein oxidative activity due to the accumulation of ROS in cells and tissues. The disruption of mitochondrial biogenesis can be marked by a decrease of peroxisome proliferator-activated receptor co-activator gamma (PGC-1a). This study aimed to determine the effect of simvastatin on skeletal muscle PGC-1a.Methods: Sixteen female Wistar rats (8-10 weeks of age) were randomized into 2 groups: (1) control group (n=8), and (2) simvastatin group(n=8). For 30 days, the simvastatin group was exposed to simvastatin at a dose of 10 mg/kg/day. Meanwhile, the control group animals only received 0.5% methyl cellulose. Gastrocnemius muscles were collected and PGC-1a levels were evaluated by using ELISA Kit.Results: Following 30 days of treatment, a significantly lower level of skeletal muscle PGC-1awas observed in the simvastatin group compared to the control group (p = .026). Conclusion: Our finding indicates that administration of simvastatin at a dose of 10 mg/kg/day for 30 days may decrease skeletal muscle PGC-1a leading to mitochondrial dysfunction in rat skeletal muscle
Simvastatin Toxicity Induces Mitochondrial Dysfunction in Rat Skeletal Muscle Zulfahmidah; Marhaen Hardjo; Syahrijuita Kadir
Indian Journal of Forensic Medicine & Toxicology Vol. 15 No. 3 (2021): Indian Journal of Forensic Medicine & Toxicology
Publisher : Institute of Medico-legal Publications Pvt Ltd

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.37506/ijfmt.v15i3.16293

Abstract

Background: Statins are the class of drugs that are widely used for lowering LDL cholesterol and as primaryand secondary prevention to cardiovascular disease. However, the widespread use of statins is constrained bythe presence of toxicity or intolerance, which affects drug control rates. The toxicity or intolerance of statinsranges from 10-15%. The most common statin toxicity is statin-associated muscle symptoms (SAMS). Theunderlying mechanisms of SAMS involve the disruption of mitochondrial biogenesis, potential membranechanges, reduced number of mitochondria, and changes in protein oxidative activity due to the accumulationof ROS in cells and tissues. The disruption of mitochondrial biogenesis can be marked by a decrease ofperoxisome proliferator-activated receptor co-activator gamma (PGC-1a). This study aimed to determine theeffect of simvastatin on skeletal muscle PGC-1a.Methods: Sixteen female Wistar rats (8-10 weeks of age) were randomized into 2 groups: (1) control group(n=8), and (2) simvastatin group(n=8). For 30 days, the simvastatin group was exposed to simvastatinat a dose of 10 mg/kg/day. Meanwhile, the control group animals only received 0.5% methyl cellulose.Gastrocnemius muscles were collected and PGC-1a levels were evaluated by using ELISA Kit.Results: Following 30 days of treatment, a significantly lower level of skeletal muscle PGC-1awas observedin the simvastatin group compared to the control group (p = .026).Conclusion: Our finding indicates that administration of simvastatin at a dose of 10 mg/kg/day for 30 daysmay decrease skeletal muscle PGC-1a leading to mitochondrial dysfunction in rat skeletal muscle.
Utilization of Nata De Durio as a Constipation Preventive (Preliminary Animal Studies) SYAM, Tri Sutriani; Ika Yustisia; Syahrijuita Kadir; Huhammad Husni Cangara; Sartini
Window of Health : Jurnal Kesehatan Vol 8 No 3 (July 2025)
Publisher : Fakultas Kesehatan Masyarakat Universitas Muslim Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.33096/woh.vi.1136

Abstract

Constipation is a symptom/problem that arises in the process of defecation, which is not smooth and irregular due to a lack of fiber intake in the body. Nata de durio is an extracellular cellulose made from durian seeds and formed from the activity of the bacterium Acetobacter xylinum, which contains high enough fiber so that it can regulate and maintain intestinal function in the defecation process. The purpose of this study is to assess the effect of using nata de durio as a natural fiber in the defecation process in vivo and to assess its effect on the transition time of feces in the small intestine of mice. The current study was an experimental study using male mice that were given distilled water as a negative control, inulin as a positive control, and nata seed de durio with doses of 0.02 gram, 0.04 gram, and 0.08 gram as a treatment group for 5 weeks. According to the findings of this study, the administration of nata de durio had a better effect on the amount of feces, weight of feces, frequency of defecation, and consistency of feces compared to the control group. The study's conclusion is that nata de durio can be used as a natural fiber in improving the defecation pattern of BALB/c male mice.