Dwi Cahyani Ratna Sari
Bagian Anatomi, Embriologi dan Antropologi, Fakultas Kedokteran Universitas Gadjah Mada

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Journal : Berkala Ilmu Kedokteran

Ethanolic extract of the Centella asiatica (L.) Urb. leaf decreases cerebellar brain-derived neurotrophic factor (BDNF) levels in rats after chronic stress Sari, Dwi Cahyani Ratna; Juananda, Desby; Ar-Rochmah, Mawaddah; Romi, Muhammad Mansyur; Arfian, Nur
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 50, No 2 (2018)
Publisher : Journal of the Medical Sciences (Berkala ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (770.994 KB) | DOI: 10.19106/JMedSci005002201801

Abstract

Chronic stress produces glucocorticoid-induced neurotoxicity that may lead to alterations of the brain-derived neurotrophic factor (BDNF) concentration in the brain. Cerebellum is known to be severely affected by glucocorticoids-associated oxidative damage. Centella asiatica (L.) Urb. may protect neurons from oxidative damage. This study aimed to investigate the effect of ethanolic extract of C. asiatica (L.) Urb. leaf on the rat cerebellar BDNF levels following stress. Twenty young-adult male Sprague Dawley rats were randomly assigned into four experimental groups. The stress control group received aquadest, and the other groups were treated with different doses of the C. asiatica (L.) Urb. extract i.e 150 (CeA150), 300 (CeA300) and 600 (CeA600) mg/kg body weight/day orally, respectively and followed by chronic footshock stress for 28 days. Upon completion of the experimental period, all animals were sacrificed and the cerebellar was isolated. The BDNF levels from the cerebellar tissue lysate was measured using ELISA. The mean BDNF levels of the cerebellar tissue in the stress control, CeA150, CeA300 and CeA600 groups were 1217.10±301.40; 771.46±241.45; 757.05±268.29; and 627.00±246.02 pg/mL, respectively. Post-hoc analysis showed a significant difference between the control and treatment groups (p< 0.05). In conclusion, the ethanolic extracts of the C. asiatica (L.) Urb. leaf decrease the cerebellar BDNF levels in rats after chronic stress.
Prolonged Kidney Ischemia-Reperfusion Injury Associates with Inflammation, Vascular Remodelling, and Myofibroblast Formation Arfian*, Nur; Ats-tsani, Hilma Kholida; Sayekti, Pratiwi Indah; Lakabela, Dwina Agrila; Amelia, Amelia; Febriyanto, Toni; Antonio, Hana Rutyana Putri; Wibisono, Dian Prasetyo; Sari, Dwi Cahyani Ratna
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 50, No 1 (2018)
Publisher : Journal of the Medical Sciences (Berkala ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (1436.153 KB) | DOI: 10.19106/JMedSci005001201801

Abstract

Prolonged kidney ischemia-reperfusion injury (IRI) is the important risk factor for leading to chronic kidney disease (CKD). Persistent hypoxia and inflammation are considered as the main pathogenesis of chronic injury, followed by myofibroblast expansion and fibrosis process. Tubular injury, cell proliferation, and vasoconstriction, as acute compensatory responses, are restored in chronic phase. The aim of the study was to investigate the relation between inflammation, vascular remodeling, and myofibroblast formation as response to ischemia injury after prolonged kidney ischemia-reperfusion (I/R). Fifteen male Swiss mice aged 3-4 months were used as kidney I/R injury model after bilateral pedicle renal clamping. Rats were divided into 3 groups with five rats in each group i.e. control group (sham operation/SO), acute I/R model (IR1), and chronic I/R model (IR12). PAS staining was used for scoring tubular injury. Fibrosis was assessed using sirius red and a-SMA immunostaining for myofibroblast expansion. PCNA and CD68 immunostaining were used for identifying cell proliferation and macrophage infiltration. RT-PCR was conducted for assessing MCP-1, HIF-1a, and ppET-1 expression, which were quantified using ImageJ software. Data were analyzed using one way ANOVA and Kruskal-Wallis test with significance level of p<0.05. Significantly increase of tubular injury score (p<0.001) and PCNA positive cell (p<0.001) in IR1 group compared to SO were observed, otherwise HIF-1a of IR12 enhanced (p<0.05). Macrophage cell count (p<0.01) and MCP-1 expression (p<0.05), were significantly increase in IR1 and IR12 injury, compared to SO. Wall thickness of arteries was significantly increase (p<0.05) as well as decrease of vascular lumen area (p<0.05), followed by enhancement of ppET-1 expression (p<0.01) in IR1 group and restored significantly (p<0.05) in IR12 group. Fibrosis fraction-area and myofibroblast expansion were significantly increase gradually from IR1 to IR12 injury (p<0.01). In conclusion, prolonged kidney I/R injury induces the sustainability of hypoxia and inflammatory response, which promotes myofibroblast formation, and decrease the response of vascular remodelling.