Fauziyatul Munawaroh
Department Of Anatomy, Faculty Of Medicine, Public Health, And Nursing, Universitas Gadjah Mada, Yogyakarta, Indonesia

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Increased blood-brain barrier permeability correlate with microglial activation at hippocampal CA1 region in acute and chronic bilateral common carotid artery ligation in rats Dian Prasetyo Wibisono; Nur Arfian; Handoyo Pramusinto; Fauziyatul Munawaroh; Yeshua Putra Krisnugraha; Daniel Agriva Tamba; Dwi Cahyani Ratna Sari
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 54, No 2 (2022)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.19106/JMedSci005402202201

Abstract

Inflammatory processes might play a key role in the pathogenesis of post-stroke epilepsy. The activation of microglia and release of vascular cell adhesion molecule-1 (VCAM1) might induce blood-brain barrier (BBB) disintegration. However, the influence of such pathomechanisms in the generation of post-stroke epilepsy is still not clear. We investigated whether cerebral ischemia exerts effects on inflammation in the hippocampus by measuring the hippocampal injury score, expression of a microglial marker, and expression of VCAM1 in rats. A total of 24 Sprague Dawley rats were randomized into four groups with 6 rats in eachgroup i.e. sham operation (SO) as control, carotid ligation 1 (GCL1) as an acute model, carotid ligation 3 (GCL3) as a subacute model, and carotid ligation 7 (GCL7) as a chronic model. Immunostaining for microglia marker (CD68) was measured in rat brain tissue sections. The VCAM1 expression was evaluated by reverse transcription-polymerase chain reaction (RT-PCR). Cerebral ischemia increased the amount of microglial immunostaining and expression of VCAM1. The hippocampal injury score and microglial immunopositivity were significantly correlated with the duration of brain ischemia. We conclude that cerebral ischemia is correlated with neuroinflammatory reaction and disturbance of BBB permeability, and the correlation of those molecular impairments with the generation of post-stroke epilepsy remains to be elucidated.
Correlation between Nephrin expression, tubular injury, and serum Creatinine level in kidney failure model with 5/6 subtotal Nephrectomy in mice M. Mansyur Romi; Dwi Cahyani Ratna Sari; Riky Setyawan; Fauziyatul Munawaroh; Nur Arfian
Indonesian Archives and Biomedical Sciences Vol 1 No 1 (2021): Indonesian Archives and Biomedical Sciences Vol 1(1): 2021
Publisher : Konsorsium Ilmu Biomedik Indonesia (KIBI)

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Abstract

Background: Chronic kidney diseases (CKD) is characterized by glomerulosclerosis, tubular injury, and proteinuria. Neprin is the one of the most important protein involved in glomerular filtration but the mechanism of nephrin expression in chronic kidney failure is not well understood. Objective: We aims to elucidate the correlation between nephrin expression with tubular injury and serum creatinine level. Methods: We performed 5/6 subtotal nephrectomy (SN) in male strain Swiss mice to induce CKD. Sham operation was performed to control group (SO) (n=8). Mice were sacrificed in day 7 (SN7; n=8) and day 28 (SN28; n=8) after operation. We measure creatinine serum level to assess renal function. Tubular injury score was quantified using Periodic Acid Schiff (PAS) staining. Reverse transcriptase PCR (RT-PCR) was carried out to examine Nephrin mRNA expression. Results: 5/6 subtotal nephrectomy induced an increased of serum creatinine level in SN7 and SN28 (p<0,01 vs SO), followed by an increased of tubular injury score in SN7 and SN28 (p<0,01 vs SO). We confirmed reduction of nephrin expression in SN28 (p<0.01 vs SO). There was a negative correlation between nephrin and tubular injury (r=0.719, p<0.01) and the positive correlation between tubular injury and serum creatinine level (r=0.891, p<0.01). However, we did not find any significant correlation between nephrin expression and serum creatinine level. Conclusion: Nephrin expression downregulation might represent renal function disturbtion in CKD.