Biomedical Sciences Doctoral Candidate Investigates Natural Product-Based Combination Therapy for Malaria Resistance News and Activities

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• Selasa, 18 Agustus 2026
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Held at the Postgraduate Meeting Room (3rd Floor, Postgraduate Building, Udayana University, Denpasar), the Doctoral Study Program in Biomedical Sciences at the Faculty of Medicine, Udayana University, conducted an open doctoral defense for candidate Dr. Putu Indah Budi Apsari, M.Si. Her dissertation is titled "Andrographolide as a Potential Agent in Artemisinin Combination Therapy to Overcome Malaria Resistance" (August 18, 2026).

 

Antimalarial resistance poses a global challenge to malaria elimination efforts worldwide. Artemisinin resistance in *Plasmodium falciparum* is characterized by a failure to eradicate the parasite or a delay in parasite clearance from the blood. Underlying mechanisms of Artemisinin resistance include mutations in the *kelch 13* (K13) gene, increased expression of *Autophagy-related gene 8* (ATG8), modulation of Reactive Oxygen Species (ROS) pathways—specifically through elevated levels of Superoxide Dismutase (SOD) and Catalase enzymes—and immune system activation. K-13 gene mutations and increased ATG8 expression play a role in regulating proteostasis and the synthesis of proteins essential for parasite survival. Reduced ROS production diminishes Artemisinin activation, thereby allowing the parasite to survive. Furthermore, immune system activation via Nuclear Factor-kappa B (NF-kB) triggers an excessive release of the cytokine Tumor Necrosis Factor-alpha (TNF-?), leading to more severe symptoms in the host. Andrographolide, an active compound derived from *Andrographis paniculata*, possesses known antimalarial activity; while numerous studies have reported its potential as an antitumor, anti-inflammatory, antioxidant, and anti-sclerotic agent, the specific mechanism by which it prevents Artemisinin resistance has not yet been fully elucidated. This study aims to unravel the mechanism by which Andrographolide prevents *Plasmodium* resistance to Artemisinin. The research employed an *in silico* docking approach using AutoDock 4.2 to evaluate biochemical reactions and ligand-receptor interactions, assessing the potential of andrographolide to inhibit oxidative stress, autophagy, and immune pathways via AutoDock 4, Biovia, and GROMACS software. An *in vivo* study utilized 20 *Mus musculus* (BALB/c) mice infected with *Plasmodium berghei*, divided into four groups: a negative control (no drug), a positive control (artesunate at 0.8 mg/30 g body weight), Treatment Group 1 (andrographolide at 10 mg/30 g body weight), and Treatment Group 2 (a combination of artemisinin and andrographolide at the same dosages). Parameters assessed included the gene expression of K13, ATG8, and NF-?B via quantitative Polymerase Chain Reaction (qPCR), catalase enzyme expression via immunohistochemistry, and parasitemia levels. Data analysis was performed using ANOVA with a significance level of p< 0.05.

 

The results demonstrated that the parent compound andrographolide, as well as its derivatives and phase 1 and 2 metabolites, exhibited strong binding affinities