Histological Changes In Kidney Research Articles

Vitamin D is involved in the effects of the intestinal flora and its related metabolite TMAO on perirenal fat and kidneys in mice with DKD

BackgroundVitamin D was shown to directly exert a protective effect on diabetic kidney disease (DKD) in our previous study. However, whether it has an effect on perirenal adipose tissue (PRAT) or the intestinal flora and its metabolites (trimethylamine N-oxide, TMAO) is unclear.MethodsDKD mice were received different concentrations of 1,25-(OH)2D3 for 2 weeks. Serum TNF-α levels and TMAO levels were detected. 16S rRNA sequencing was used to analyze gut microbiota. qPCR was used to detect the expression of TLR4, NF-Κb, PGC1α, and UCP-1 in kidney and adipose tissue. Histological changes in kidney and perirenal adipose tissue were observed using HE, PAS, Masson and oil red staining. Immunofluorescence and immunohistochemistry were used to detect the expression of VDR, PGC1α, podocin, and UCP-1 in kidney and adipose tissue. Electron microscopy was used to observe the pathological changes in the kidney. VDR knockout mice were constructed to observe the changes in the gut and adipose tissue, and immunofluorescence and immunohistochemistry were used to detect the expression of UCP-1 and collagen IV in the kidney.Results1,25-(OH)2D3 could improve the dysbiosis of the intestinal flora of mice with DKD, increase the abundance of beneficial bacteria, decrease the abundance of harmful bacteria, reduce the pathological changes in the kidney, reduce fat infiltration, and downregulate the expression of TLR4 and NF-κB in kidneys. The serum TMAO concentration in mice with DKD was significantly higher than that of the control group, and was significantly positively correlated with the urine ACR. In addition, vitamin D stimulated the expression of the surface markers PGC1α, UCP-1 and VDR in the PRAT in DKD mice, and TMAO downregulated the expression of PRAT and renal VDR.ConclusionsThe protective effect of 1,25-(OH)2D3 in DKD mice may affect the intestinal flora and its related metabolite TMAO on perirenal fat and kidneys.

Metabolic Analysis and Renal Protective Effects of Linagliptin and Empagliflozin in Alport Syndrome.

We previously demonstrated that Empagliflozin (Empa), a sodium-glucose cotransporter-2 (SGLT2) inhibitor, reduces intrarenal lipid accumulation and slows kidney function decline in experimental Alport syndrome (AS). In this study, we aimed to evaluate the renal protective benefits of Linagliptin (Lina), a dipeptidyl peptidase-4 (DPP4) inhibitor in AS and compare it to Empa. Metabolite distribution in kidney cortices was assessed using mass spectrometry imaging. We examined albuminuria and histological changes in kidneys from AS mice treated with Lina and/or Empa or vehicle. Several metabolites, including adrenic acid (AdA) and glucose, were increased in renal cortices of AS mice when compared to wildtype (WT) mice, while eicosapentaenoic acid (EPA) levels were decreased. In addition, a redistribution of AdA from the glomerular compartment in WT mice to the tubulointerstitial compartment in AS mice was observed. Both Lina and Empa treatments were found to reduce albuminuria, to extend the survival of AS mice for about 10 days, and to decrease glomerulosclerosis and tubulointerstitial fibrosis compared to WT mice. There were no significant differences with regard to the renal phenotype observed between Empa and Lina treated AS mice, and the combination of Lina and Empa was not superior to individual treatments. In vitro experiments revealed that DPP4 is expressed in podocytes and tubular cells derived from both AS and WT mice. Differently from what we have reported for Empa, Lina treatment was found to reduce glucose-driven respiration in AS tubular cells, but not in AS podocytes. Renal expression patterns and spatial distribution of several metabolites differ in AS compared to WT mice. While Lina and Empa treatments similarly partially slow the progression of kidney disease in AS, the metabolic mechanisms conferring the protective effect may be different.

Kefir mitigates renal damage caused by zearalenone in female wistar rats by reducing oxidative stress

The estrogen-like mycotoxin zearalenone (ZEA) was popularly occurred in several food and feeds, posing threats to human and animal health. ZEA induced renal toxicity and caused oxidative stress. In the current study, the protecting effect of kefir administration against ZEA-induced renal damage in rats was explored. Rats were divided into 4 groups, each consisting of 5 animals. For the initial 7 days, they were orally administered sterile milk (200 μL/day). Subsequently, during the second week, the groups were exposed to kefir (200 μL/day), ZEA (40 mg/kg b.w./day) and a combination of kefir and ZEA. The biochemical parameters, kidney histological changes and ZEA residue were assessed. Kefir supplementation enhanced the antioxidant enzymes in the kidney, such as superoxide dismutase, catalase and glutathione peroxidase activities, which increased by 1.2, 4 and 20 folds, respectively, relative to the ZEA group. Remarkably, the concomitant administration kefir + ZEA suppressed ZEA residues in both serum and kidney. Additionally, serum levels of blood urea nitrogen, uric acid and renal malondialdehyde decreased by 22, 65 and 54%, respectively, in the kefir + ZEA group; while, the creatinine content increased by around 60%. Rats co-treated with kefir showed a normal kidney histological architecture contrary to tissues alterations mediated in the ZEA group. These results suggest that kefir may showed a protective effect on the kidneys, mitigating ZEA-induced acute toxicity in rats.

Induction of micronuclei in blood and histopathological alterations in gill, kidney and liver of Channa punctatus (Bloch, 1793) exposed to copper sulphate

Copper is one of the most toxic metals to fish and causes cytotoxic, mutagenic and carcinogenic effects. The accumulation of copper in an aquatic environment directly impacts man and the aquatic ecosystem. The present study aimed to determine the effect of copper sulphate (CuSO4) accumulation on the induction of micronuclei in blood and histological changes in kidney and liver of the fish Channa punctatus. The test chemical LC50 was determined after 96 hours during the first experiment. Later in the second experiment, the test animal was exposed to three sub-lethal concentrations of CuSO4 [0.1 mg/l (96 h-LC50/40), 0.2 mg/l (96 h-LC50/20) and 0.4 mg/l (96 h-LC50/10)]. Physico chemical parameters of the test medium, such as pH, temperature, hardness, alkalinity, and dissolved oxygen, were observed throughout the experiment, and all values were within the ranges necessary for the fish's survival. At intervals of 7, 14, 21, and 28 days, the control (without any test chemical) and copper sulphate exposed Groups' blood, liver, kidney, and gill tissues were taken to evaluate changes in genotoxic and histological parameters. Micronuclei (MN) induction and nuclear abnormalities (NAs) were observed at regular intervals. After 28 days, the MN frequency in Groups 1, 2, 3, and 4 was 0.78±0.006, 8.40±0.052, 10.37±0.098 and 10.90±0.024 respectively. A significant (P< 0.05) rise in MN frequencies and NAs indicated fish erythrocytes' DNA damage. Histological analysis of the liver, kidney, and gills revealed serious tissue injury such as necrosis, vacuolization, and degeneration after 28 days in the exposed Groups. The present study observed changes due to genotoxicity and histology, giving the most comprehensive understanding of CuSO4 stress on the fish C. punctatus and its risks to human health.

Imperatorin ameliorates kidney injury in diabetic mice by regulating the TGF-β/Smad2/3 signaling axis, epithelial-to-mesenchymal transition, and renal inflammation

Diabetic nephropathy (DN) is a serious concern in patients with diabetes mellitus. Prolonged hyperglycemia induces oxidative damage, chronic inflammation, and build-up of extracellular matrix (ECM) components in the renal cells, leading to kidney structural and functional changes. Imperatorin (IMP) is a naturally occurring furanocoumarin derivative with proven antioxidative and anti-inflammatory properties. We investigated whether IMP could improve DN and employed high glucose (HG)-induced HK-2 cells and high-fat diet-fed streptozotocin (HFD/STZ)-generated DN experimental model in C57BL/6 J mice. In vitro, IMP effectively reduced the HG-activated reactive oxygen species generation, disturbance in the mitochondrial membrane potential (MMP) and epithelial-to-mesenchymal transition (EMT)-related markers, and the transforming growth factor (TGF)-β and collagen 1 expression in HK-2 cells. In vivo, we found an elevation of serum creatinine, kidney histology alterations, and collagen build-up in the kidneys of the DN control group. Also, we found that altered expression of EMT-related markers, upregulation of the TGF-β/Smad2/3 axis, and elevated pro-inflammatory molecules, TNF-α, IL-1β, IL-18 and phospho–NF–kB (p65) in the DN control group. IMP treatment did not significantly reduce the blood glucose level compared to the DN control group. However, IMP treatment effectively improved renal damage by ameliorating kidney histological changes and serum renal injury markers. IMP treatment restored renal antioxidants and exhibited anti-inflammatory effects in the kidneys. Moreover, the abnormal manifestation of EMT-related attributes and elevated levels of TGF-β, phospho-Smad2/3, and collagen 1 were also normalized in the IMP treatment group. Our findings highlight that IMP may be a potential candidate for treating DN.

Chronic kidney disease in a murine model of non-alcoholic steatohepatitis (NASH)

Clinical studies suggest that non-alcoholic steatohepatitis (NASH) is an independent risk factor for chronic kidney disease (CKD), but causality and mechanisms linking these two major diseases are lacking. To assess whether NASH can induce CKD, we have characterized kidney function, histological features, transcriptomic and lipidomic profiles in a well-validated murine NASH model. Mice with NASH progressively developed significant podocyte foot process effacement, proteinuria, glomerulosclerosis, tubular epithelial cell injury, lipid accumulation, and interstitial fibrosis. The progression of kidney fibrosis paralleled the severity of the histologic NASH-activity score. Significantly, we confirmed the causal link between NASH and CKD by orthotopic liver transplantation, which attenuated proteinuria, kidney dysfunction, and fibrosis compared with control sham operated mice. Transcriptomic analysis of mouse kidney cortices revealed differentially expressed genes that were highly enriched in mitochondrial dysfunction, lipid metabolic process, and insulin signaling pathways in NASH-induced CKD. Lipidomic analysis of kidney cortices further revealed that phospholipids and sphingolipids were the most significantly changed lipid species. Notably, we found similar kidney histological changes in human NASH and CKD. Thus, our results confirm a causative role of NASH in the development of CKD, reveal potential pathophysiologic mechanisms of NASH-induced kidney injury, and established a valuable model to study the pathogenesis of NASH-associated CKD. This is an important feature of fatty liver disease that has been largely overlooked but has clinical and prognostic importance.

Evaluation of Hemotoxic, Hepatotoxic and Nephrotoxic Potential of Profenofos-based Insecticide in Freshwater Labeo rohita Fish at Low Concentrations

Profenofos, an organophosphate, is a major pollutant that pollutes freshwater bodies, causing significant impacts on fish health. Objective: Present study was performed to assess the toxicological impacts of pesticide profenofos on hematological, biochemical and histological alterations in different organs of Labeo rohita. Methods: Fish were divided in three groups. Group one was treated as control while second and third groups were exposed to 0.6 mg/L and 1.2 mg/L profenofos respectively for 28 days. Results: Results revealed that MCV, MCHC, MCH, RDW-SD, PCT, PDW, HGB, RBC and HCT levels were significantly reduced. WBC, RDW, PLT, MPV, neutrophils, lymphocytes, monocytes and eosinophils were increased as compared to pesticide free group. Biochemical results showed significant increase in cholesterol, triglycerides, AST, albumin, A/G ratio, HDL T3, T4, blood glucose, creatinine and urea levels were documented while levels of LDL, VLDL, ALT, total proteins, globulin, TSH and blood urea nitrogen (BUN) decreased significantly in exposed fish. Furthermore, histological changes in kidney, gills and liver of fish showed degenerative effects after exposure to profenofos in both concentrations. Conclusions: The present study concluded that profenofos resulted in widespread toxic effects on aquatic organisms specially fish.

Role of Glimepiride in Ameliorating Histological Changes in kidney of Experimentally Induced Diabetes mellitus in Rats

Role of Glimepiride in Ameliorating Histological Changes in kidney of Experimentally Induced Diabetes mellitus in Rats

Melatonin alleviates renal injury in diabetic rats by regulating autophagy.

Melatonin (MLT) is a biologically active indoleamine involved in regulating various biological rhythms, which is deficient in individuals with Type 2 diabetes. The present study examined the effects of MLT on diabetic neuropathy (DN). Diabetic rats received MLT treatment for 12weeks, after which changes in kidney histology, oxidative damage, mitochondrial morphology and autophagy were measured. The glucose tolerance‑ and isoflurane tolerance‑area under the curve (AUC) values and the relative renal weight index (RI) in the diabetes mellitus (DM) group of rats were significantly higher compared with those in the control group. A significant increase in malondialdehyde (MDA) content, and decreases in the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH‑Px) and GSH were demonstrated in the kidneys of DM rats compared with those in the control rats. Histological staining of DM rat kidney tissue with hematoxylin and eosin, Masson's trichome and Periodic acid‑Schiff demonstrated glomerular and tubule lesions, and an increase in collagen compared with control rats. Protein expression levels of LC3II, P62, collagen IV (COL‑IV) and α‑SMA were increased in DM rats and HG‑induced NRK‑52E cells compared with those in the control groups. Phosphorylation of AMPK was reduced, whereas phosphorylation of PI3K, Akt and mTOR were increased invivo and invitro. Notably, MLT treatment significantly reduced glucose tolerance‑AUC and RI, decreased MDA content, and increased SOD, CAT, GSH‑Px and GSH activity. Glomerular and tubule lesions improved, collagen was decreased and mitochondrial damage was alleviated by MLT treatment. MLT treatment also decreased the protein expression levels of LC3II, P62 and COL‑IV, whereas the phosphorylation of AMPK was significantly increased, which inhibited the phosphorylation of PI3K, AKT and mTOR invivo and invitro. These results demonstrated that MLT protects against DN and NRK‑52E cell injury through inhibiting oxidative damage and regulating autophagy via the PI3K/AKT/mTOR signaling pathway.

Angiopoietin-like 4 (ANGPTL4) Suppression Ameliorates Lupus Nephritis in MRL/lpr Mice by Inactivating NLRP3 Inflammasome and Inhibiting Inflammatory Response.

Lupus nephritis (LN) refers to the injury caused by systemic lupus erythematosus (SLE) involving the kidneys. A previous study identified angiopoietin-like protein 4 (ANGPTL4) as a novel urinary biomarker for tracking disease activity in LN. To investigate the detailed role and regulatory mechanism of ANGPTL4 in experimental models of LN. MRL/lpr mice 11-week-old were injected with adeno-associated virus (AAV)-mediated ANGPTL4 short hairpin RNA (shRNA). At 16 and 20 weeks of age, 24-h urine samples were harvested to measure proteinuria levels. After the mice were sacrificed, blood and kidney tissues were harvested to examine serum creatinine (cr) and blood urea nitrogen (BUN) levels, kidney histological changes, and pro-inflammatory cytokine production. Additionally, the levels of NLRP3 inflammasome-associated molecules in mouse renal tissues were detected to clarify the underlying mechanism. The AAV-sh-ANGPTL4 injection significantly reduced the proteinuria, cr, and BUN levels in MRL/lpr mice. ANGPTL4 silencing ameliorated glomerular, tubular, and interstitial damage in mice, mitigating the pathological alternations of LN. In addition, ANGPTL4 knockdown repressed pro-inflammatory cytokine production in the kidneys. Mechanically, ANGPTL4 suppression inhibited NLRP3 inflammasome expression in renal tissues of mice. ANGPTL4 silencing inhibits the NLRP3 inflammasome-mediated inflammatory response, thereby ameliorating LN in MRL/lpr mice.

Bee Venom Causes Oxidative Stress, Biochemical and Histopathological Changes in the Kidney of Mice.

Accidents with venomous bees are a serious worldwide health concern. Since the kidney has been reported as the main venom-target organ, the present study was undertaken to investigate the in vivo nephrotoxic effect of Algerian bee venom (ABV) (Apis mellifera intermissa) collected in the middle east of Algeria. A preliminary study was performed on ABV to identify the ABV using SDS-PAGE analysis and to determine the in vivo intraperitoneal median lethal dose (LD50) using the Probit analysis test. In vivo nephrotoxic effect was assessed through the determination of physiological and kidney biochemical markers in mice intraperitoneally injected with ABV at doses of 0.76 (D1); 1.14 (D2) and 2.29 mg/kg body weight (bwt) (D3), corresponding respectively to LD50/15, LD50/10, and LD50/5 (i.p. LD50=11.48 mg/kg bwt) for seven consecutive days. Results revealed a marked decrease in body weight gain and food intake, and an increase in absolute and relative kidney weights in ABV D2 and D3 treated mice compared with controls. Furthermore, ABV D2 and D3 resulted in a significant increase in serum creatinine, urea, and uric acid. ABV-induced oxidative stress was evidenced by a significant increase in kidney MDA level, and a significant depletion in kidney GSH level, and catalase activity. Meanwhile, no marked changes in the above-mentioned parameters were noticed in ABV D1. Accordingly, the adverse nephrotoxic effect of ABV was proved by the dose-dependent kidney histological changes. In summary, the results of the present study evidence that ABV at doses of 1.14 (D2) and 2.28 mg/kg body weight (bwt) can cause marked changes in kidney biochemical and major antioxidant markers, and histological architecture.

Association between Kidney Donor Risk Index, kidney graft function and histological changes in early post-transplant graft biopsy.

Proper assessment of donor organ quality is crucial for optimal kidney allocation and best long-term outcomes. The aim of this study was to analyze the association between the Kidney Donor Risk Index (KDRI) and histological parameters in early post-transplant graft biopsy in a Polish cohort of kidney transplant recipients. In 418 consecutive kidney transplant recipients, a histological evaluation of very early [at median 11 (9-13) post-transplant day] protocol core needle biopsy was performed and analyzed according to the Banff classification. Subjects were divided into quartiles of the KDRI value. Kidney graft function, patient and graft survival were also analyzed over a median follow-up period of 44 (26-56) months. There was a significant trend toward greater intensity of chronic histology changes along the KDRI quartiles (χ2=20.8; P<.001), including interstitial fibrosis, tubular atrophy, mesangial matrix increase and arteriolar hyalinosis. Stepwise multivariate regression analysis revealed that only higher KDRI value independently increased the severity of chronic graft injury (rpartial=0.340, P<.001). KDRI values were valuable in the determination of both early and long-term graft function. The KDRI values correlate with chronic histological changes found in early post-implantation kidney biopsies and can also be helpful in the prediction of graft outcome.

Remission of lupus nephritis: the trajectory of histological response in successfully treated patients

ObjectiveThis study investigated changes in kidney histology over time in patients with lupus nephritis (LN) undergoing immunosuppressive treatment.MethodsPatients with proliferative±membranous LN were studied. After a diagnostic kidney biopsy (Bx1), patients...

The role of ZnO NPs loaded with metformin NPs in kidney histological changes in Rats with Diabetic Nephropathy

The role of ZnO NPs loaded with metformin NPs in kidney histological changes in Rats with Diabetic Nephropathy

Nephroprotective effects of Candesartan Cilexetil against Cyclosporine A-induced nephrotoxicity in a rat model.

Cyclosporine A (CsA), a well-known immunosuppressive drug, has been prescribed after organ transplantation and in a variety of disorders with an immunological origin. Nephrotoxicity is one of the most frequently stated problems associated with CsA, and therefore the treatment with CsA remains a big challenge. This study sets out to assess the ameliorative influences of Candesartan Cilexetil (CC) on oxidative stress and the nephrotoxic effect of CsA in a rat model. Twenty-four Wister Albino rats, 7-8-week-old, weighing 150-250g, were randomly categorized into three groups (eight animals in each group). These groups were the (1) CsA-treated group, (2) vehicle-treated group, and (3) CC-treated group. Bodyweights were assessed at the start and end of experiments. Renal function test and levels of glutathione peroxidase 1 catalase -CAT (Gpx1), catalase (CAT), superoxide dismutase (SOD), interleukin -2 (IL-2), and malondialdehyde (MDA) were investigated in renal tissues. Histological changes in kidneys were also evaluated. Data showed that levels of urea and creatinine in serum and levels of IL-2 and MDA in renal tissues were elevated in the CsA-treated group, with severe histological changes compared with the control group. Furthermore, tissue levels of Gpx1, CAT, and SOD were significantly decreased in CsA-treated in comparison with the control group. Treatment with CC for the rats subjected to CSA resulted in a marked reduction in levels of serum urea and creatinine and tissue levels of IL-2 and MDA. Levels of Gpx1, CAT, and SOD in renal tissues were greater in the CC-treatment group compared with the CsA-treated group. CC treatment reduced the deterioration of renal morphology compared with CsA treatment. The findings of this study suggest that CC could prevent CSA-induced nephrotoxicity through its anti-inflammatory and antioxidant influences. Considerably more work needs to be done to determine the mechanistic insight behind the ameliorative effect of CC.

The Potential Protective Effect and Underlying Mechanisms of Physiological Unconjugated Hyperbilirubinemia Mediated by UGT1A1 Antisense Oligonucleotide Therapy in a Mouse Model of Cyclosporine A-Induced Chronic Kidney Disease.

Cyclosporine A (CSA) is an immunosuppressive drug that has improved transplant survival rates. However, its use is often limited because it is thought to be linked to the development of chronic kidney disease after kidney transplants. This study aimed to investigate the protective effects and underlying mechanisms of physiological unconjugated (UC) hyperbilirubinemia mediated by UGT1A1 antisense oligonucleotide in a mouse model of CsA-induced chronic kidney disease, and match these with that of chitosan (CH) as a natural chelator against kidney injury. In the current study, CsA-treated mice were given an intravenous injection of UGT1A1 antisense morpholino oligonucleotide (16 µg/kg) every third day for 14 days. In serum samples, bilirubin, creatinine, and urea were determined. Markers of oxidative stress, antioxidant activities, and mRNA expression of target genes PPAR-α, cFn, eNOS, NF-B, AT1-R, ETA-R, Kim-1, and NGAL were measured in the kidney tissues. Moreover, histopathological examinations were carried out on the kidney tissue. Physiological UC hyperbilirubinemia could be a promising protective strategy against CsA-induced kidney disease in transplant recipients. UGT1A1 antisense oligonucleotide-induced physiological UC hyperbilirubinemia serum significantly protected against CsA-induced kidney dysfunction. UCB acts as a signaling molecule that protects against kidney disease through different mechanisms, including antioxidant, anti-inflammatory, and hormonal action, by activating nuclear hormone receptors (PPAR-α). Moreover, it significantly downregulated mRNA expression of NF-kB, ETA-R, iNOS, AT1-R, cFn, Kim-1, and NGAL in the kidney tissue and alleviated CsA-induced kidney histological changes in CsA-treated mice.

Nephrotoxicity of gasoline fumes in male albino rat: a mechanism-based approach study

Nephrotoxicity of gasoline fumes has been documented, but the mechanisms underlying the toxicity remain vague. This study determined the residue of gasoline components in the kidney of 72 male albino rats with a view to providing the basis for a detailed understanding of the nephrotoxicity of gasoline fumes. The rats were randomized into 6 groups and daily exposed to distilled water (control) or gasoline fumes for 1, 3, 5, 7 and 9 h for 10 weeks. Some standard clinical blood biochemistry, activities of some kidney antioxidant and membrane-bound ATPase enzymes and kidney histological changes were examined. Gasoline hydrocarbons were extracted, identified and quantified in the kidney of rats with Gas Chromatography-Mass Spectrometry (GC-MS). Significant (p < 0.05) changes were observed in the biochemical parameters examined in the blood and kidney of the exposed rats compared to the control. Residues of some gasoline metabolites including 2,3-diphenylcyclopropyl) methyl phenyl sulfoxide; Cyclotrisiloxane and 2.2-Paracyclophane were identified in the kidney of rats exposed to gasoline fumes. The kidney of the exposed rats also displayed mild histological changes. Retention of some hydrocarbons in the kidney of rats exposed to gasoline fumes could potentially result in oxidative stress capable of inducing renal dysfunction. Key policy highlights Continuous exposure to gasoline fumes for varying hours over a period of time may result in the retention of some gasoline hydrocarbons and metabolites in the kidney of the exposed animal. Presence of gasoline hydrocarbons and metabolites in the kidney may induce a high production of reactive oxygen species and consequently lead to oxidative damage to the organ. Metabolic process of gasoline hydrocarbons in the kidney of the exposed animal varies with the hours of exposure.

The effect of syzygium polyanthum (wight) extract in histological changes of kidney in diabetic mice model

Introduction: Diabetes mellitus, or hyperglycemia, is one of the risk factors for atherosclerosis, causing disruption of blood flow through arterial plaque formation and atherosclerosis. Diabetic kidney disease (DKD) is the most common cause of chronic and end-stage renal disease (CKD and ESRD) worldwide and is a stronger predictor of mortality in people with diabetes. Although the concept that the kidney plays a key role in glucose balance is not new, it is only recently that this organ has been viewed as a potential therapeutic target. This study aimed to assess the potential effect of Syzygium polyanthum extract in DKD mice model. Methods: We administrated Syzygium polyanthum extract for 2-weeks to alloxan-induced diabetic mice. Results: Treatment with Syzygium polyanthum extract reduced blood glucose levels in dose dependency (2,62mg/20g/day, 5,24mg/20g/day, and 7,86mg/20g/day). Histological analysis showed that Syzygium polyanthum extract significantly (p&lt;0,05) improved the kidney lesions in low dose, but did not show a significant effect on inflammatory cell at glomerulus. Conclusion: Syzygium polyanthum extract has potential to improve the kidney lesion in low dose and showed therapeutic potential in DKD treatment.

Psoriatic nephropathy: A histopathological update

Background and Aims : Psoriasis is one of the most common dermatoses and accounts for 12 to 15% of all skin diseases. Visceral pathology, manifested in patients with psoriasis, has been attracting increasing attention from many researchers for many years. One of the central places in the visceral lesions in psoriasis is the pathology of the kidneys - psoriatic nephropathy. Our aim was to examine histological changes of kidneys in patients with psoriasis vulgaris.

Bone Marrow Mesenchymal Stem Cells (BMSCs)-Exosomes Carrying MicroRNA-965 Attenuates Allogeneic Renal Transplant Rejection Through Regulation of Janus Kinase/Signal Transducers and Activators of Transcription 3 (JAK/STAT3)

This study intends to evaluate the potential effect of BMSC-derived exosomes (exo) on the rejection of allogeneic kidney transplantation in a rat model. BMSCs were cultured and their exos were collected for characterization, in which the expression of miR-965 was detected by PCR. Rats received orthotopic kidney transplantation and treated with exos or PBS followed by analysis of serum creatinine and BUN, inflammatory cell infiltration, renal fibrosis and vascular wall fibrosis by immunohistochemistry staining, JAK2/STAT3 phosphorylation by Western-blot, the inflammatory factor level by ELISA kit, and CD4+ cells differentiation by flow cytometry. miR-965 was enriched in BMSC-derived exo. Treatment with exo ameliorated the allograft rejection, improved renal function, and reduced the histological changes of kidney. In addition, exosomal treatment decreased the level of serum inflammatory cytokines, and altered T cell subpopulations. Meanwhile, fibrosis and neointima formation was reduced as demonstrated by related protein expression and signaling pathways was inactivated in the presence of exos. In conclusion, the miR-965 derived from BMSC-exos mitigated the renal allograft rejection through JAK/STAT3 signaling.