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All Journal JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA Jurnal Layanan Masyarakat (Journal of Public Service)
Chrismawan Ardianto
Department Of Pharmacy Practice, Faculty Of Pharmacy, Universitas Airlangga, Surabaya
Humanities Chemistry Decision Sciences, Operations Research & Management Education Environmental Science Health Professions Medicine & Pharmacology Social Sciences Other

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Journal : JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA

 1 
The Effect of Serotonin-Norepinephrine Reuptake Inhibitor Milnacipran on Anxiety-like Behaviors in Diabetic Mice Tuhfatul Ulya; Chrismawan Ardianto; Mahardian Rahmadi; Dewi Wara Shinta; Junaidi Khotib
JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA Vol. 8 No. 3 (2021): JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jfiki.v8i32021.200-206

Abstract

Background: Diabetes mellitus is a chronic disease that causes neuronal plasticity and increased hypothalamic pituitary adrenal (HPA) axis of stress disorders. The change in metabolism is reportedly associated with inadequate response to antianxiety and antidepressant agents. Objective: This study aimed to determine the effect of milnacipran antidepressants on anxiety-like behavior in mice with diabetes mellitus. Methods: Male ICR mice were divided into naive, stress, diabetes mellitus (DM), DM + stress groups to measure anxiety-like behavior. Diabetes mellitus was induced using alloxan, and electric footshock stress was used as a stressor for 14 consecutive days. Anxiety-like behavior was measured using the light-dark box (LDB) and elevated plus maze (EPM) test at days 0, 7 and 14. The antidepressant milnacipran (MIL) was given for 7 days, on days 8 to 14. On day 14, evaluation of anxiety-like behavior after administration of MIL was carried out in all groups using LDB and EPM tests. Results: The results showed that administration of milnacipran effectively ameliorated anxiety-like behavior in the non-DM, but not in the DM group, using the LDB test. A similar result was demonstrated in the EPM test showing the non-DM group's attenuation after milnacipran administration. Conclusion: The present results indicate that there is an inadequate attenuation of the anxiety-like behavior after treatment with milnacipran in diabetes conditions.
Molecular Docking of Active Compound of Lavandula angustifolia Mill Essential Oil against N-methyl-D-aspartate (NMDA) Receptor Baiq Risky Wahyu Lisnasari; Aniek Setiya Budiatin; Chrismawan Ardianto; Junaidi Khotib
JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA Vol. 9 No. 1 (2022): JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jfiki.v9i12022.75-81

Abstract

Background: Lavender oil is widely known to possess a relaxant effect to relieve stress, anxiety, and depression. Linalyl acetate, linalool, geranyl acetate, and β-caryophyllene were the major constituents of lavender oil that potentially act on NMDAR (N-methyl-d-aspartate receptors), and emerging targets in the treatment of depression. Objective: This study aims to predict the binding of lavender compounds to NMDA receptors using an in silico model. Methods: The ligands of the docking study were four major chemical compounds of lavender oil, i.e., linalyl acetate, linalool, geranyl acetate, and β-caryophyllene. 5YE was defined as a native ligand, while memantine, an NMDAR antagonist, was used as a reference ligand. The NMDAR structure was taken from Protein Data Bank (ID 5H8Q), while the lavender compound was sketched in Chem3D. Autodock 4.2 was used to perform the docking analysis. Results: The result showed that beta-caryophyllene had the most potent interaction with NMDAR (free binding energy was -8.02 kcal/mol and inhibitory constant was 1.32 µM). Conclusion: The docking results suggest that beta-caryophyllene could be an NMDAR antagonist and be developed as a treatment for depression.
Effect of Fenofibrate as PPARα Agonist in Suppressing the Development of Oxaliplatin-Induced Peripheral Neuropathy via TRPA1 Modulation Alma Nuril Aliyah; Pingkan Aprilia; Anak Agung Sagung Dyah Pramesti; Tarisya Dinda Saraya; Galuh Laksatrisna Pide; I Nengah Budi Sumartha; Luke Wongso; Samirah; Mahardian Rahmadi; Muhammad Zaki Bin Ramli; Chrismawan Ardianto
JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA Vol. 10 No. 2 (2023): JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA
Publisher : Universitas Airlangga

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.20473/jfiki.v10i22023.257-265

Abstract

Background: CIPN (Chemotherapy-induced Peripheral Neuropathy) primarily affects the sensory system and is accompanied by pain, autonomic dysfunction, and motor impairments. Alterations of intracellular second messengers at the supraspinal level in CIPN needed to be explored more. In addition, there is a lack of evidence regarding implications for the supraspinal area through the propagation of pain via the ascending pathway. Objective: In this study, we evaluated the effect of fenofibrate as a PPARα agonist in suppressing the development of CIPN. Methods: Twenty-four mice were distributed to the normal control group, neuropathy group, and neuropathy with the treatment of fenofibrate 75 and 150 mg/kg groups, resulting in 6 animals per group. Oxaliplatin was injected on days 0, 2, 4, and 6. The hot plate test was performed before the oxaliplatin administration and then continued on the 7th, 14th, and 21st days. Thalamus tissues were collected to measure the TRPA1 mRNA expression using qPCR. Results: Fenofibrate 75 mg/kg co-treatment with oxaliplatin tended to prevent the enhancement of oxaliplatin-induced thermal hyperalgesia in hind-paw withdrawal and rubbing responses. Furthermore, fenofibrate 75 and 150 mg/kg co-treatment with oxaliplatin significantly reduced the relative TRPA1 mRNA expression but did not modulate the relative BDNF mRNA expression in the thalamus. Conclusion: PPARα agonist has a potential effect in suppressing the development of CIPN. However, given the various perspectives on the role of neurotrophins in CIPN, additional non-clinical investigations, are needed to provide more insight into other mechanisms of CIPN and the role of PPAR agonists.
Co-Authors Alma Nuril Aliyah Anak Agung Sagung Dyah Pramesti Arina Dery Puspitasari Baiq Risky Wahyu Lisnasari Budiatin, Aniek Setiya Dewi Wara Shinta Galuh Laksatrisna Pide I Nengah Budi Sumartha Junaidi Khotib Luke Wongso Mahardian Rahmadi Mahardian Rahmadi Muhammad Zaki Bin Ramli Pingkan Aprilia Samirah Suharjono Suharjono Tarisya Dinda Saraya Tuhfatul Ulya