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All Journal Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Indonesian Journal of Biotechnology
Dian Prasetyo Wibisono
Division Of Neurosurgery, Department Of Surgery, Faculty Of Medicine, Public Health And Nursing, Universitas Gadjah Mada/Dr. Sardjito General Hospital, Yogyakarta
Biochemistry, Genetics & Molecular Biology Immunology & microbiology Materials Science & Nanotechnology Neuroscience

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Inverse correlation of kidney interstitial cells expansion with hemoglobin level and erythropoietin expression in single and repeated kidney ischemic/reperfusion injury in mice Dian Prasetyo Wibisono; Nur Arfian; Muhammad Mansyur Romi; Wiwit Ananda Wahyu Setyaningsih; Dwi Cahyani Ratna Sari
Indonesian Journal of Biotechnology Vol 24, No 1 (2019)
Publisher : Universitas Gadjah Mada

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (727.855 KB) | DOI: 10.22146/ijbiotech.43989

Abstract

Ischemic/reperfusion injury (IRI) causes acute kidney injury that may lead to chronic kidney disease. We investigated the correlation between kidney interstitial cells expansion, hemoglobin level, and erythropoietin expression as the chronic effects of single and repeated kidney IRI in mice. We created an IRI model using male Swiss mice by clamping the bilateral renal pedicles. Subjects were divided into four groups that contained six mice each: control/sham operation, single acute IRI, single chronic IRI, and repeated IRI. Our results showed that the single chronic and repeated IRI groups significantly increased the tubular injury score, decreased the hemoglobin level, and increased erythropoietin expression compared with the control. Lower hemoglobin levels in all of the groups compared with the control was associated with erythropoietin resistance. In single chronic and repeated kidney IRI, there were decreased creatinine levels compared with the control. The decreased creatinine levels from the single acute IRI group to the single chronic IRI group, suggesting a repair phase of IRI starting on day 7 occurred in the single chronic IRI group. A macrophage marker, CD68, and an inflammatory mediator marker, MCP-1, significantly increased in all IR groups, indicating inflammation occurred due to IRI. In conclusion, chronic and repeated kidney IRI induced interstitial cells expansion and inflammation associated with anemia.
Prolonged Kidney Ischemia-Reperfusion Injury Associates with Inflammation, Vascular Remodelling, and Myofibroblast Formation Nur Arfian*; Hilma Kholida Ats-tsani; Pratiwi Indah Sayekti; Dwina Agrila Lakabela; Amelia Amelia; Toni Febriyanto; Hana Rutyana Putri Antonio; Dian Prasetyo Wibisono; Dwi Cahyani Ratna Sari
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. 
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.
Co-Authors Amelia Amelia Daniel Agriva Tamba Dwi Cahyani Ratna Sari Dwina Agrila Lakabela Fauziyatul Munawaroh Hana Rutyana Putri Antonio Handoyo Pramusinto Hilma Kholida Ats-tsani Muhammad Mansyur Romi Nur Arfian Pratiwi Indah Sayekti Toni Febriyanto Wiwit Ananda Wahyu Setyaningsih Yeshua Putra Krisnugraha