scholarly journals Ginseng Ameliorates Effect of Prolonged Use of Omeprazole in Rat Renal Cortex through Decreasing Inflammation, Fibrosis and Apoptosis

2020 ◽  
Author(s):  
Dina Ali Maher Abdel Dayem ◽  
Ahmed Sayed Mahmoud ◽  
Azza Hussein Ali ◽  
Nashwa Fathy Gamal El-Tahawy
Keyword(s):  
Renal Cortex ◽  
Morphological Changes ◽  
Histological Study ◽  
Protective Role ◽  
Basement Membranes ◽  
Serum Urea ◽  
Tubulointerstitial Injury ◽  
Vascular Congestion ◽  
Apoptotic Effects

AbstractOmeprazole is used in acid-related gastrointestinal disorders but has prolonged usage adverse effects. The aim was to study changes in renal cortex following chronic Omeprazole administration and the possible protective role of ginseng. Rats were divided into control (C-), Ginseng (G-), omeprazole (OM-), and omeprazole-ginseng (OM-G) groups. Serum urea and creatinine levels and 24-hours urine-protein were determined. Kidneys were processed for histological study. Serum urea and creatinine and 24-hours protein were significantly higher in OM-group compared to controls and significantly decreased in OM-G group comparing to OM-group. OM-group showed significant glomerular and tubulointerstitial injury with vascular congestion, inflammatory cell infiltration, partial or complete damage of apical brush border of most tubules, interrupted basement membranes of glomerular capillaries and tubules, marked increase in collagen deposition, and significant increases in COX-2 and caspase-3 immune-expression. Co-administration of ginseng with omeprazole resulted in marked and significant improvement of these morphological changes.ConclusionOmeprazole induced renal functional and morphological changes through inflammatory reaction, induction of fibrosis, cellular degeneration and apoptosis. Co-administration of ginseng ameliorated these effects through its anti-inflammatory, anti-fibrotic, and anti-apoptotic effects.

P0523PROTECTIVE ROLE OF REGULATORY B CELLS ON THE RENAL TISSUE REPAIRMEN AFTER ISCHEMIA REPERCUSSION INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yokota Yunosuke ◽  
Goh Kodama ◽  
Sakuya Itou ◽  
Yosuke Nakayama ◽  
Nobukazu Komatsu ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Renal Function ◽  
B Cells ◽  
Interleukin 10 ◽  
Renal Tissue ◽  
Protective Role ◽  
Regulatory B Cells ◽  
Tubulointerstitial Injury ◽  
Iri Model

Abstract Background and Aims Acute kidney injury (AKI), even if followed by renal recovery, is a risk factor for the future development of chronic kidney disease (CKD) and end- stage renal disease. It has been postulated that interleukin-10 (IL-10)-producing Regulatory B cells (Breg) play an important role for the tissue repairment in several tissues and organs. Basically, protective role of Breg has been reported in inflammatory bowel disease. In the kidney, it has been shown that IL-10 suppresses renal function decline and improves renal prognosis in IRI model, a typical model of AKI. However, the identity of Breg in the kidney and their origin have not been clarified. Further, how the Breg works during the transition from AKI to CKD is not known. Therefore, first we investigated whether Breg existed in renal tissue on the progression from AKI to CKD in IRI model mice. Further, we performed splenectomy, and examined the renal injury, Breg, and plasma IL-10 levels in this model. Method To examine the existence of Breg in the kidney of IRI model, we used 8-10 weeks-old GFP / IL-10 mice based on C57BL / 6J mice. They are reporter mice for IL-10 producing cells, and can visualize IL-10 producing cells under a fluorescence microscope without fluorescent immunostaining. We prepared following three groups, sham, IRI (unilateral), and IRI + SN (splenectomy) groups. Mice were anesthetized with chloral hydrate (4 g/kg,, intraperitoneal). After making a midline incision, exposed a blood vessel of the left renal pedicles and clamped it for 30 min by clips. one day, 7 days, and 14 days after the surgery, mice were sacrificed, and renal function and plasma IL-10 levels as well as tissue damages by PAS and Masson’s Trichrome staining were assessed. Tissue IL-10-producing cells were detected by flow cytometry. Results There was no difference of plasma IL-10 levels and renal tubulointerstitial injury in IRI group and IRI+SN group on day 1 after IRI. However, on day 7 and day 14, plasma IL-10 levels became gradually higher in IRI group, and SN decreased the increase in IL-10 levels. Tubulointerstitial injury was induced by IRI and SN further worsened tubular damages. Serum Cr and BUN levels were not different in three groups due to normal right kidney. On day 1, number of IL-10-producing B cells increased in the spleen and renal medulla in IRI group confirmed by flow cytometry, which was completely diminished by SN, suggesting that origin of the infiltrated Breg might be spleen, thereby being involved in the protective role in IRI injury in the kidney. Conclusion We report for the first time that Breg might be recruited from spleen by AKI, which may be one of the mechanisms to prevent the progression to CKD.

Protective Role of Transforming Growth Factorβ(TGFβ) in Tumor-Induced Degradation of Basement Membranes

1990 ◽  
Vol 371 (2) ◽  
pp. 687-692 ◽  
Author(s):  
Krešimir PAVELIĆ ◽  
Neda DESPOT ◽  
Sonja LEVANAT ◽  
Tino ČASL
Keyword(s):  
Protective Role ◽  
Basement Membranes

Nitric oxide-dependent pro-oxidant and pro-apoptotic effect of metallothioneins in HL-60 cells challenged with cupric nitrilotriacetate

2001 ◽  
Vol 354 (2) ◽  
pp. 397-406 ◽  
Author(s):  
Shang-Xi LIU ◽  
Kazuaki KAWAI ◽  
Vladimir A. TYURIN ◽  
Yulia Y. TYURINA ◽  
Grigory G. BORISENKO ◽  
...  
Keyword(s):  
Dna Cleavage ◽  
Caspase 3 ◽  
Protective Role ◽  
Membrane Phospholipids ◽  
No Donor ◽  
Redox Active ◽  
Apoptotic Effect ◽  
Transition And Heavy Metals ◽  
Apoptotic Effects

Intracellular safeguarding functions of metallothioneins (MTs) include sequestering transition and heavy metals, scavenging free radicals and protecting against electrophiles. We report that MT protection against Cu-induced cytotoxicity can be reversed and pro-oxidant and pro-apoptotic effects can be induced in HL-60 cells exposed to NO. We demonstrate that in ZnCl2-pretreated HL-60 cells loaded with copper nitrilotriacetate (Cu-NTA), exposure to an NO donor, S-nitroso-N-acetyl penicillamine, resulted in S-nitrosylation and oxidation of MT cysteines. This disruption of MT Cu-binding thiolate clusters caused loosening and release of redox-active Cu, enhanced redox-cycling activity of Cu and increased peroxidation of major classes of membrane phospholipids. We also found that Cu-induced oxidative stress in ZnCl2-pretreated/Cu-NTA-loaded HL-60 cells was accompanied by apoptosis documented by characteristic changes of nuclear morphology, internucleosomal DNA cleavage, externalization of phosphatidylserine, release of cytochrome c from mitochondria into cytosol and activation of caspase-3. We conclude that in Cu-challenged cells, NO can reverse the protective role of MTs and convert them into pro-oxidant, pro-apoptotic implements.

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