Malaria is still a global health problem around the world particularly in Indonesia. Chloroquine is one of the anti-malarial drugs which is still used in Indonesia. The aim of this research is to know the synergic effect of Chloroquine and N-Acetyl Cysteine towards parasitemia and erythrocyte malondyaldehyde levels in mice infected with Plasmodium berghei. This was an experimental research using Plasmodium berghei and BALB/c strain mice, 6−8 weeks old, with body weight 20−30 grams. After infected with Plasmodium berghei, the mice were divided into eight (8) groups: control, chloroquine, NAC 0.25 mg/gBb; NAC 0.5 mg/gBb; NAC 1 mg/gBb and combined drugs of chloroquine and NAC 0.25 mg/gBb; NAC 0.5 mg/gBb; NAC 1 mg/gBb. On the 3rd, 5th, and 7th day after treatment, the mice were killed and their parasitemia and Malondialdehyde (MDA) levels were measured. By using MANOVA and Tukey HSD test, a signifi cant difference in parasitemia level was found between the control and chloroquine group, as well as the control and combined drug groups. In the NAC groups, there was no decrease. The decrease of MDA level began on the 7th day. It can be concluded that there was a synergic effect between the chloroquine and N-Acetyl Cysteine in decreasing parasitemia and malondyaldehyde levels in mice BALB/c infected with Plasmodium berghei.
Peningkatan permeabilitas sel eritrosit yang terinfeksi Plasmodium falciparum terhadap ion dan makromolekul diketahui sebagai mekanisme parasit untuk memenuhi nutrisi dalam proses pertumbuhan. Peningkatan permeabilitas terhadap kalsium masih merupakan hal yang kontradiktif dalam peranannya meningkatkan pertumbuhan Plasmodium falciparum dalam sel eritrosit. Tujuan dari penelitian ini adalah mengetahui peningkatan pertumbuhan Plasmodium falciparum dalam sel eritrosit pasca pemberian kalsium. Biakan primer Plasmodium falciparum dalam medium biakan RPMI 1640 yang menghasilkan parasitemia 15%, dilakukan inokulasi untuk pembuatan subkultur yang menghasilkan parasitemia 2% dan dilakukan pembagian untuk kelompok perlakuan pemberian kalsium dan kontrol (ML 10%) dengan replikasi 3 kali. Pengamatan dilakukan hari pertama sampai hari ke-6 setelah perlakuan. Pengamatan pertumbuhan dilakukan dengan parameter parasitemia, bentuk skizon, hemolisis dan kalsium intraseluler. Hasil penelitian menunjukkan bahwa pemberian kalsium menghasilkan peningkatan tertinggi jumlah total rerata parasitemia (11,09 ± 4,01) (Rerata ± SD), bentuk skizon (23,52 ± 10,83), hemolisis (0,278 ± 0,03) dan kalsium intraseluler (6,55 ± 1,88), dibandingkan dengan media biakan kontrol (ML 10%). Analisis T-test (α= 0,05) menghasilkan perbedaan yang signifikan pada parameter parasitemia, bentuk skizon, hemolisis tetapi tidak memberikan perberbedaan yang signifikan pada parameter kalsium intraseluler.
Metabolic syndrome is a group of several risk factors consist of hypertension, dyslipidemia, glucose intolerance disorder, obesity, and has a relationship with CVD pathomechanism. WHO was report in 2003 more than 300 million adult in the world suffered from obesity. The role of adipose tissue in infectious diseases and adipocyte quality changes after exposure to pathogen has not been revealed. On the other hand, the prevalence of infectious diseases in developing country is still high. Previous studies proved a relationship between infection of Toxoplasma gondii and tissue dysfunction. Profilin is a membrane component of Toxoplasma gondii that able to stimulate expression of proinflammation cytokines through TLR-11 upregulation, and predicted able to trigger the adipocyte dysfunction. The aim of this study is to knows the effect of profilin exposure in vitro on subcutaneous adipocyte to the expression of IL-6 and TNF-α. The measurement of IL-6 and TNF- levels was done by ELISA technique. The result showed profilin exposure doses 5, 15 and 25 ng / ml increasing IL-6. Profilin exposure cause adipocyte dysfunction through the increasing proinflammatory adipocytokine levels as pathomechanism of metabolic syndrome associated with adipose tissue.
ABSTRAKInflamasi kronis pada asma merupakan salah satu faktor yang mempengaruhi keparahan, eksaserbasi, dan remodeling jalan nafas yang ditandai peningkatan apoptosis epitel bronkiolus. Interleukin (IL)-4 merupakan salah satu sitokin tipe Th2 yang merupakan petanda proses inflamasi. Tujuan penelitian ini adalah untuk membuktikan hubungan antara ekspresi IL-4 dan apoptosis epitel pada bronkiolus mencit asma. Penelitian dilakukan dengan desain randomized control group menggunakan 18 mencit galur Balb/c yang dibagi dalam kelompok asma dan kontrol. Kelompok asma disensitisasi dengan ovalbumin secara intraperitoneal pada hari ke-0 dan 14, diikuti dengan cara inhalasi setiap 2-3 hari selama 6 minggu. Ekspresi IL-4 pada bronkiolus diperiksa dengan metode imunohistokimia, sedangkan apoptosis epitel bronkiolus dengan metode TUNEL. Analisis statistik menggunakan independent sample t-test, Mann-Whitney U test, dan regresi linier dengan interval kepercayaan 95%. Jumlah apoptosis epitel bronkiolus dan ekspresi IL-4 meningkat bermakna pada 2 kelompok asma (p=0,000).Terdapat korelasi positif kuat (r=0,78; r =0,56, p=0,012, y=4,28+0,58x) antara IL-4 dan apoptosis epitel pada bronkiolus. Peningkatan ekspresi IL-4 mempengaruhi peningkatan apoptosis epitel bronkiolus, namun bukan merupakan satu-satunya variabel yang mempengaruhi peningkatan apoptosis epitel bronkiolus.Kata Kunci : Asma, apoptosis epitel, bronkiolus, IL-4, ovalbumin ABSTRACT Chronic inflammation in asthma is one of the factors that influence the severity, exacerbation, and airway remodeling marked increase in bronchial epithelial apoptosis. Interleukin (IL) -4 is a cytokine which is a marker of
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.