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Pharmacokinetics Profile of Chitosan Nanoparticles in Chronic Lead-induced Toxicity Rats Model Marianti, Aditya; Amalina, Nur Dina; Mursiti, Sri; Sitompul, Faya Nuralda; Futri, Shafira Septiana; Negara, Legendra Gantar; Sholehah, Intan Kharyna; Asmorowati, Dian Sri; Astari, Putri Dyah
Biosaintifika: Journal of Biology & Biology Education Vol. 16 No. 1 (2024): April 2024
Publisher : Universitas Negeri Semarang

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.15294/biosaintifika.v15i1.1857

Abstract

Chronic lead exposure induces ROS accumulation which causes physiological disorders. Chelation therapy has been widely used to overcome lead poisoning since it exerts only a few side effects. Nano chitosan prevents lead poisoning by inhibiting ROS. This study examined the pharmacokinetics of nano chitosan in chronic lead-induced toxicity animal models and the mechanism of action pathway using the bioinformatic approach, The area under the curve was estimated to be 12110.13 ± 7709.37 μg/mL hours using the pharmacokinetic model, and the Cmax was 82.34 ± 5.64 μg/mL. The Tmax and t½ calculations were 22.68 ± 11.67 and 80.47 ± 60.58 hours respectively. Chitosan nanoparticles regulated VEGFA, FGF2, and LGALS3 which plausibly played a substantial role in chronic lead exposure. However, chitosan is not suitable for oral administration due to its low gastrointestinal solubility. These characteristics make chitosan nanoparticles have the prospect of being developed as a supplement so that they can contribute to overcoming the negative impacts of chronic lead poisoning.
Inhibitory Effects of Petai Peel Extract Gel on Tyrosinase and TRP1 Gene Expression in UVB-Exposed Mouse Skin Hutabarat, Nenny Lynda Caroline; Subchan, Prastyowati; Putra, Agung; Amalina, Nur Dina; Sitompul, Faya Nuralda
International Journal of Cell and Biomedical Science Vol 2 No 6 (2023)
Publisher : Stem Cell and Cancer Research (SCCR)

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.59278/cbs.v2i6.43

Abstract

Background: UVB irradiation can induce the formation of Reactive Oxygen Species (ROS), which causes the activation of melanin synthesis through the activation of tyrosinase and tyrosinase-related protein-1 (TRP1). Secondary metabolites in stink bean peel extract inhibit ROS production due to exposure to UVB rays. This study aims to determine the effect of administering stink bean peel extract gel on the expression of the tyrosinase and TRp1 genes in mouse skin tissue exposed to UVB. Method: The research design was a posttest-only control group with a completely randomized design method. The samples studied were 24 mice exposed to UVB light with a wavelength of 302 nm and an energy of 390mJ/cm2/day 3 times a week for 2 weeks. This research was carried out in four groups: the healthy group, the negative control group, treatment 1 (T1) with 10% stink bean peel extract gel, and treatment 2 (T2) with 20% stink bean peel extract gel. Tyrosinase and TRP1 gene expression were analyzed using qRT-PCR. Results: qRT-PCR analysis showed that there was a significant decrease in tyrosinase and TRP1 gene expression between groups T1 (tyrosinase 3,19±2,12 and TRP1 4,96±3,42) and T2 (tyrosinase 0,65±0,44 and TRP1 2,22±1,18) compared to negative control (tyrosinase 17,92±3,77 and TRP1 35,91±4,52). Conclusion: The administration of stink bean peel extract gel has shown promising results in reducing the expression of tyrosinase and TRP1 genes in hyperpigmentation mice exposed to UVB light. This suggests that stink bean peel extract could be a safe and effective therapeutic approach for preventing UVB-induced hyperpigmentation.