Management Of Diabetic Nephropathy Research Articles

Moringa isothiocyanate-1 mitigates the damage of oxidative stress and apoptosis in diabetic nephropathy mice.

Diabetic nephropathy (DN) is a prevalent cause of end-stage kidney disease worldwide. Moringa isothiocyanate-1 (MIC-1) has shown potential for DN management, however, the exact mechanisms remain unclear. This research intended to evaluate the impact and mechanism of MIC-1 on DN. Six C57BLKS/J-db/m mice served as controls. Eighteen C57BLKS/J-db/db mice were randomly separated into three groups: db/db, db/db + irbesartan (IBS), and db/db + MIC-1. Three weeks post-drug administration, the body weight and kidney weight of mice in each group were measured. Concurrently, serum creatinine (Scr), urine albumin, insulin, glycosylated hemoglobin (GHb), oxidative stress-, and inflammatory-related factors were determined. Additionally, the pathological injury, apoptosis, apoptosis-related markers, NLRP3, and ASC levels in the kidney tissues were examined utilizing H&E, Masson, PAS, TUNEL staining, and Western blot. MIC-1 decreased the body weight, kidney weight, the levels of Glu, Scr, and urine albumin in db/db mice. Moreover, MIC-1 significantly suppressed the levels of MDA, insulin, GHb, TNF-α, IL-1β, and IL-6, while increased the activities of SOD, CAT, and GPX in the serum of db/db mice. MIC-1 also mitigated the kidney tissue injury in db/db mice. Western blot assay showed that MIC-1 enhanced the Bcl-2 level and suppressed the Bax, cleaved caspase-3, cleaved caspase-9, NLRP3, ASC, and caspase-1 levels of the kidney tissues in db/db mice. MIC-1 ameliorated the kidney injury in DN mice, and its mechanism may be associated with the suppression of renal cell apoptosis, oxidative stress, and inflammatory responses.

Analysis of clinical evidence on traditional Chinese medicine for the treatment of diabetic nephropathy: a comprehensive review with evidence mapping.

This study aims to map evidence from Randomized Controlled Trials (RCTs) and systematic reviews/Meta-analyses concerning the treatment of Diabetic Nephropathy (DN) with Traditional Chinese Medicine (TCM), understand the distribution of evidence in this field, and summarize the efficacy and existing problems of TCM in treating DN. The intention is to provide evidence-based data for TCM in preventing and treating DN and to offer a reference for defining future research directions. Comprehensive searches of major databases were performed, spanning from January 2016 to May 2023, to include clinical RCTs and systematic reviews/Meta-analyses of TCM in treating DN. The analysis encompasses the publishing trend of clinical studies, the staging of research subjects, TCM syndrome differentiation, study scale, intervention plans, and outcome indicators. Methodological quality of systematic reviews was evaluated using the AMSTAR (Assessment of Multiple Systematic Reviews) checklist, and evidence distribution characteristics were analyzed using a combination of text and charts. A total of 1926 RCTs and 110 systematic reviews/Meta-analyses were included. The majority of studies focused on stage III DN, with Qi-Yin deficiency being the predominant syndrome type, and sample sizes most commonly ranging from 60 to 100. The TCM intervention durations were primarily between 12-24 weeks. Therapeutic measures mainly consisted of Chinese herbal decoctions and patented Chinese medicines, with a substantial focus on clinical efficacy rate, TCM symptomatology, and renal function indicators, while attention to quality of life, dosage of Western medicine, and disease progression was inadequate. Systematic reviews mostly scored between 5 and 8 on the AMSTAR scale, and evidence from 94 studies indicated potential positive effects. DN represents a significant health challenge, particularly for the elderly, with TCM showing promise in symptom alleviation and renal protection. Yet, the field is marred by research inconsistencies and methodological shortcomings. Future investigations should prioritize the development of standardized outcome sets tailored to DN, carefully select evaluation indicators that reflect TCM's unique intervention strategies, and aim to improve the robustness of clinical evidence. Emphasizing TCM's foundational theories while incorporating advanced scientific technologies will be essential for innovating research methodologies and uncovering the mechanisms underlying TCM's efficacy in DN management.

Biomarkers and signaling pathways of diabetic nephropathy and peripheral neuropathy: possible therapeutic intervention of rutin and quercetin.

Diabetic nephropathy and peripheral neuropathy are the two main complications of chronic diabetes that contribute to high morbidity and mortality. These conditions are characterized by the dysregulation of multiple molecular signaling pathways and the presence of specific biomarkers such as inflammatory cytokines, indicators of oxidative stress, and components of the renin-angiotensin system. In this review, we systematically collected and collated the relevant information from MEDLINE, EMBASE, ELSEVIER, PUBMED, GOOGLE, WEB OF SCIENCE, and SCOPUS databases. This review was conceived with primary objective of revealing the functions of these biomarkers and signaling pathways in the initiation and progression of diabetic nephropathy and peripheral neuropathy. We also highlighted the potential therapeutic effectiveness of rutin and quercetin, two plant-derived flavonoids known for their antioxidant and anti-inflammatory properties. The findings of our study demonstrated that both flavonoids can regulate important disease-promoting systems, such as inflammation, oxidative stress, and dysregulation of the renin-angiotensin system. Importantly, rutin and quercetin have shown protective benefits against nephropathy and neuropathy in diabetic animal models, suggesting them as potential therapeutic agents. These findings provide a solid foundation for further comprehensive investigations and clinical trials to evaluate the potential of rutin and quercetin in the management of diabetic nephropathy and peripheral neuropathy. This may contribute to the development of more efficient and comprehensive treatment approaches for diabetes-associated complications.

Improving the identification and management of diabetic nephropathy in patients with diabetes in primary care.

Diabetic nephropathy is the leading cause of renal failure in the United States. Screening for albuminuria in individuals with diabetes is critical to identify the early stages of DKD. Prompt identification and management of DKD improves patient outcomes, increases life expectancy, and decreases health care costs. The DKD screening rate for patients ≥18 years of age with diabetes at the project site was 29%, below the national benchmark of 90%. Patients diagnosed with DKD were not receiving appropriate management. This quality-improvement project used a standardized protocol consisting of a checklist and educational initiatives to improve DKD identification and management. The Knowledge-to-Action Framework was used for this project at a primary care practice in the southeastern United States. Data collection included demographic data, DKD screening with urine albumin-to-creatine ratio, diagnosis rates, DKD treatment with angiotensin-converting enzyme inhibitor (ACEi) or angiotensin II receptor blocker (ARB), and a sodium-glucose cotransporter-2 inhibitor (SGLT2i) reviewed 6 months before and after intervention. Evidence-based interventions included a DKD educational in-service for clinical staff, creation of a standardized protocol through a checklist for screening and appropriate management of DKD, and implementation of patient educational handouts. Diabetic kidney disease screening rates increased by 100%, patients diagnosed with DKD decreased by 8%, patients with DKD on ACEi/ARB increased by 39%, and patients with DKD on SGLT2i increased by 15%. Implementation of a standardized protocol through a checklist and providing patient education on DKD can improve DKD identification/management.

The crucial role of community pharmacists in balancing the impact of statins on kidney function in patients with diabetes mellitus: Recommendations for awareness, recognition, and management of diabetic nephropathy

The crucial role of community pharmacists in balancing the impact of statins on kidney function in patients with diabetes mellitus: Recommendations for awareness, recognition, and management of diabetic nephropathy

Circular RNA COL1A2 Mediates High Glucose-Induced Oxidative Stress and Pyroptosis by Regulating MiR-424-5p/SGK1 in Diabetic Nephropathy

Diabetic nephropathy (DN) represents a major diabetes-related complication, which could undermine renal function. CircCOL1A2 has been previously reported to show abnormal expression during DN. However, its functional role in the progression of DN, as well as the potential molecular mechanisms, remains unclear. The present work examined the expression of circCOL1A2 in the plasma of DN patients, and employed high glucose (HG)-challenged HK-2 cells as the in vitro cell model of hyperglycemia (HG)-induced DN. CircCOL1A2 was silenced using siRNA in HK-2 cells to clarify the functional engagement of circCOL1A2 in HG-induced DN. We examined the roles of circCOL1A2 in regulating oxidative stress by measuring reactive oxygen species (ROS), lipid peroxidation, and superoxide dismutase (SOD) levels. Besides, the effects of circCOL1A2 silencing on pyroptosis were investigated by RT-qPCR, western blot (WB), and ELISA assays. StarBase (version 2.0) was used to identify the downstream effector of circCOL1A2, and their interactions were further verified through dual-luciferase reporter analysis, RNA pull-down assays, and RNA immunoprecipitation (RIP) assay. CircCOL1A2 was highly expressed in DN patients and HG-induced HK-2 cells. Knocking down circCOL1A2 alleviated oxidative stress and pyroptosis upon HG treatment. In addition, we demonstrated that circCOL1A2 knockdown could promote miR-424-5p expression while inhibiting Serum/Glucocorticoid Regulated Kinase 1 (SGK1) level. Furthermore, miR-424-5p inhibitor or SGK1 overexpression impaired the effects of circCOL1A2 knockdown on HG-induced oxidative stress and pyroptosis. Hence, our results demonstrated that the circCOL1A2 mediates HG-exposed pyroptosis and oxidative stress through modulating miR-424-5p/SGK1 axis in diabetic nephropathy, indicating that silencing circCOL1A2 is a potential intervention strategy for DN management.

Identification and management of diabetic nephropathy

Identification and management of diabetic nephropathy

Metformin suppresses LRG1 and TGFβ1/ALK1-induced angiogenesis and protects against ultrastructural changes in rat diabetic nephropathy

Diabetic nephropathy (DN) has high prevalence and poor prognosis which make it a research priority for scientists. Since metformin, a hypoglycaemic drug, has been found to prolong the survival of mice with DN. This study aims at investigating the molecular mechanisms leading to DN in rats and to explore the role of leucine-rich α-2-glycoprotein-1 (LRG1), activin-like kinase1 (ALK1), and transforming growth factor–β (TGFβ1) in the pathologic alterations seen in DN. The aim was also extended to explore the protective action of metformin against DN in rats and its influence on LRG1and ALK1/TGFβ1 induced renal angiogenesis. 24 male rats were used. Rats were assigned as, the vehicle group, the diabetic control group and diabetic + metformin (100 and 200 mg/kg) groups. Kidney samples were processed for histopathology, immunohistochemistry and biochemical analysis. Bioinformatic analysis of studied proteins was done to determine protein-protein interactions. Metformin reduced serum urea and creatinine significantly, decreased the inflammatory cytokine levels and reduced LRG1, TGFβ1, ALK1 and vascular endothelial growth factor (VEGF) proteins in rat kidneys. Bioinformatic analysis revealed interactions between the studied proteins. Metformin alleviated the histopathological changes observed in the diabetic rats such as the glomerular surface area and increased Bowman’s space diameter. Metformin groups showed decreased VEGF immunostaining compared to diabetic group. Metformin shows promising renoprotective effects in diabetic model that was at least partly mediated by downregulation of LRG1 and TGFβ1/ALK1-induced renal angiogenesis. These results further explain the molecular mechanism of metformin in DN management.

A Project work on Recent approches in the Treatment of Diabetic Nepheropathy

Renal failure is a common long-torm complication of diabetes mellitus. Stages of diabetic nephropathy have been described that characterize its clinical course. Diabetic nephropathy develops secondary to long- changes that damage the glomeruli’s. Therapy that focuses on the control of glomerular pressures and systemic hypertension can slow the progression of proteinuria and deterioration of renal function. Angiotensin converting enzyme (ACE) inhibitors and calcium channel blockers have been demonstrated to be effective in the management of diabetic nephropathy. A systematic approach to the patient with diabetes with help identify those individuals early in the course of disease when proper therapy may be most helpful. Diabetic nephropathy is the leading cause of chronic renal disease and a major cause of cardiovascular mortality. Diabetic nephropathy has been categorized into stages: micro albuminuria and macro albuminuria. The cut-off values of micro- and macro albuminuria are arbitrary and their values have been questioned. Subjects in the upper-normal range of albuminuria seem to be at high risk of progression to micro- or macro albuminuria and they also had a higher blood pressure than normoalbuminuric subjects in the lower norm albuminuria range. Diabetic nephropathy screening is made by measuring albumin in spot urine. If abnormal, it should be confirmed in two out three samples collected in a three to six-months interval. Additionally, it is recommended that glomerular filtration rate be routinely estimated for appropriate screening of nephropathy, because some patients present a decreased glomerular filtration rate when urine albumin values are in the normal range. The two main risk factors for diabetic nephropathy are hyperglycemia and arterial hypertension, but the genetic susceptibility in both type 1 and type 2 diabetes is of great importance. Other risk factors are smoking, dyslipidemia, proteinuria, glomerular hyper filtration and dietary factors. Nephropathy is pathologically characterized in individuals with type 1 diabetes by thickening of glomerular and tubular basal membranes, with progressive meningeal expansion (diffuse or nodular) leading to progressive reduction of glomerular filtration surface. Concurrent interstitial morphological alterations and hyalinization of afferent and efferent glomerular arterioles also occur. Podocytes abnormalities also appear to be involved in the glomerulosclerosis process. In patients with type 2 diabetes, renal lesions are heterogeneous and more complex than in individuals with type 1 diabetes. Treatment of diabetic nephropathy is based on a multiple risk factor approach, and the goal is retarding the development or progression of the disease and to decrease the subject's increased risk of cardiovascular disease. Achieving the best metabolic control, treating hypertension (<130/80 mmHg) and dyslipidemia (LDL cholesterol <100 mg/dl), using drugs that block the renin-angiotensin-aldosterone system, are effective strategies for preventing the development of micro albuminuria, delaying the progression to more advanced stages of nephropathy and reducing cardiovascular mortality in patients with diabetes.

Potential Therapeutic Effect of TLR4-Primed Mesenchymal Stem Cells in Lessening Kidney Damages in Rat Model of Diabetic Nephropathy

Background and Aims: Substantial damage to the kidney tissue and diabetic nephropathy (DN) can be caused by chronic hyperglycemic conditions and exposure to a high level of blood glucose. In the current study, we explored the capability of adipose-derived mesenchymal stem cells (ADSCs) and Toll-like receptor-4-primed mesenchymal stem cells (TLR4-primed MSCs) on kidney regeneration, resolution of inflammation, and alleviation of diabetic nephropathy in DN in the rats.
 Materials and Methods: STZ-induced diabetic rat models were divided into 5 subgroups, including 1) DN group, 2) DN group received insulin, 3) DN group received human foreskin fibroblast (DN-HFF), 4) DN group received single pulse of 1×106 cells of MSCs and 5) DN group received single pulse of TLR4-primed MScs. Thereafter, biochemical and histological analysis was performed on DN-model groups. Biochemical analysis exhibited a blood urea nitrogen level recovery in both MSCs and TLR4-primed MSCs-treated groups. Administration of MSCs also up-regulated mRNA expression of Bcl-xL, while the expression of Bax was significantly down-regulated.
 Results: Histological and molecular results showed that TLR4-primed MSCs have an anti-inflammatory and anti-apoptotic effect on inflamed kidneys and effectively reduced DN indicators in the TLR4-primed MSCs group compared to the unprimed MSCs group.
 Conclusion: Priming with LPS improves the therapeutic effects of MSCs in the rat model of DN, consequently lessening the symptoms of DN rats. This study proposes that primed MSCs can be served as a potential therapeutic approach in diabetes mellitus and DN management.

Effect of Costus pictus per se and in combination with Metformin and Enalapril in streptozotocin induced diabetic nephropathy in rats.

The present study was designed to investigate the effect of methanolic extract of Costus pictus (MECP) per se and in combination with drugs (Metformin and Enalapril) used in clinical practice in streptozotocin (STZ) induced diabetic nephropathy (DN) in rats. Diabetes was induced in male Wistar rats by a single injection of STZ (50mg/kg i.p.). After 28 days diabetic rats were divided into six groups. Two groups were treated with MECP (200mg/kg p.o.), MECP (400mg/kg p.o.) respectively; one group was treated with metformin (225mg/kg), enalapril (3.2mg/kg) combination; and two groups were treated with a combination of metformin, enalapril and MECP (200mg/kg) and combination of metformin, enalapril and MECP (400mg/kg) respectively. One group was kept as diabetic control. At the end of the study, body weight, kidney weight, and kidney hypertrophy index were evaluated. Biochemical and antioxidant parameters were evaluated. TGF-β levels in serum were estimated. Histopathology of the kidney was also studied. The combination therapy showed a significant increase in the body weight, lowered blood glucose levels and ameliorated kidney hypertrophy index in STZ induced diabetic nephropathy in rats. It also normalized the altered levels of serum and urine parameters. Histopathological evaluation revealed that combination therapy reduced the vacuolar degeneration of tubules. The results indicate that combination therapy of metformin, enalapril, and MECP has beneficial effects in management of diabetic nephropathy.

Plant Calotropis gigantea: Management of Diabetic Nephropathy in Experimentally Induced Diabetes in Rats

The research study designed to investigate the nephroprotective efficiency of Calotropis gigantea stem bark extract. Streptozotocin (60 mg/kg/ i.p) diabetes model was used to evaluate the Nephropathy potential of Calotropis gigantea in animals. After single administration of STZ nephropathic complication develops within four weeks. Nephropathy was assessed by blood urea nitrogen, increasing serum creatinine level, microproteinuria, lipid alteration and high renal oxidative stress. Calotropis gigantea stem bark extract shows prominent nephroprotective effect at high dose (500 mg/kg p.o) as compared to low dose treatment (200 mg/kg p.o) in experimentally induced diabetic nephropathy in rats. The present study indicated the plant having of medicinally significant bioactive constituents that shows tremendous nephroprotective effect. It is concluded that stem bark extract of Calotropis gigantea had a role in diabetes control and impedes the continuation of diabetes-induced experimental nephropathy.

Efficacy and Safety of Tripterygium wilfordii Polyglycosides Versus Valsartan in Management of Diabetic Nephropathy

Efficacy and Safety of Tripterygium wilfordii Polyglycosides Versus Valsartan in Management of Diabetic Nephropathy

Herbal Drugs used in the Management of Diabetic Nephropathy

Diabetic nephropathy (DN) or diabetic kidney disease refers to the deterioration of kidney function seen in chronic type 1 and type 2 diabetes mellitus patients. The progression of the disease is known to occur in a series of stages and is linked to glycemic and blood pressure control. Diabetis nephropathy is a kidney disease. In normal conditions the function of kidney help to regulate fluids and salts balance in the body, which is vital for control blood pressure (BP) and protect cardiovascular condition. In Diabetic condition increases blood sugar levels in high, this sugar level increase long time of the period then these high glucose levels can damage various regions of the body including the cardiac system and kidney. Damaging of kidney that results or this condition is termed as diabetes nephropathy. The average incidence of diabetic nephropathy is high (3% per year) during the first 10 to 20 years after diabetes onset. Typically, it takes 15 years for small blood vessels in organs like kidney, eyes and nerves to get affected. It is estimated that more than 20 and up to 40% of diabetic patients will develop chronic kidney disease (CKD).

POS-187 PROGNOSTIC ROLES OF URINARY TUBULAR INJURY MARKERS IN DIABETIC NEPHROPATHY

Tubular damage is common in the pathology of diabetic nephropathy (DN) and the severity of interstitial fibrosis and tubular atrophy associates with DN progression. Diabetic patients could have decreased kidney function without overt proteinuria, which highlighted the importance of tubular injury markers in DN management. However, the prognostic roles of urinary tubular injury markers are not well established. This retrospective study sought to correlate current clinically used urinary tubular injury markers with DN pathological features and renal outcomes.

Spop ameliorates diabetic nephropathy through restraining NLRP3 inflammasome

Diabetic nephropathy (DN) is one of the most common causes for end-stage renal disease without effective therapies available. NLR family, pyrin domain-containing 3 (NLRP3) inflammasome possesses a fundamental effect to facilitate the pathogenesis of DN. Unfortunately, how NLRP3 inflammasome is mediated still remains largely unclear. In the present study, an E3 ubiquitin ligase Speckle-type BTB-POZ protein (Spop) was identified as a suppressor of NLRP3 inflammasome. We first showed that Spop expression was extensively down-regulated in kidney of DN patients, which was confirmed in kidney of streptozotocin (STZ)-challenged mice and in high glucose (HG)-stimulated podocytes. Intriguingly, we showed that conditional knockout (cKO) of Spop in podocytes considerably accelerated renal dysfunction and pathological changes in the glomerulus of STZ-induced mice with DN, along with severe podocyte injury. Furthermore, Spop specific ablation in podocytes dramatically facilitated inflammatory response in glomeruli of DN mice via enhancing NLRP3 inflammasome and nuclear factor κB (NF-κB) signaling pathways, which were confirmed in HG-cultured podocytes. Notably, our findings indicated that Spop directly interacted with NLRP3. More importantly, Spop promoted NLRP3 degradation via elevating K48-linked polyubiquitination of NLRP3. Collectively, our findings disclosed a mechanisms through which Spop limited NLRP3 inflammasome under HG condition, and illustrated that Spop may be a novel therapeutic target to suppress NLRP3 inflammasome, contributing to the DN management.

Casticin Alleviates the Proliferation and Extracellular Matrix Deposition in Glomerular Mesangial Cells Induced by High Levels of Glucose

Diabetic nephropathy is a common complication of diabetes associated with defects in the extracellular matrix. However, its precise mechanism remains to be explored. Casticin (3′, 5-dihydroxy-3, 4′, 6, 7-tetramethoxyl flavone) is a bioactive component of Fructus vitexis known to exhibit many biological and pharmacological effects. Herein, we have explored the role and mechanism of casticin-mediated amelioration of diabetic nephropathy. Using a high glucose induced glomerular mesangial cell model, we report casticin inhibition of high glucose induced excessive glomerular mesangial cell proliferation, inflammation, and extracellular matrix deposition. Casticin suppressed TGF-β1/Smad pathway, and therefore alleviated the proliferation and extracellular matrix deposition of glomerular mesangial cells. These data suggest that casticin could serve as a promising drug for the management of diabetic nephropathy.

Sitagliptin's renoprotective effect in a diabetic nephropathy model in rats: The potential role of PI3K/AKT pathway.

Management of diabetic nephropathy (DN) is far from satisfactory. There is a rising role of the involvement of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway in the pathogenesis of DN. This study aimed at investigating the renoprotective effects of PI3K/AKT pathway via sitagliptin in a rat model of DN. Thirty-two male Wistar rats were divided into four groups (eight rats each): (I) control, (II) sitagliptin, (III) DN, and (IV) DN + sitagliptin. Fasting blood glucose (FBG), kidney index, and kidney function tests in both blood and urine were measured. The levels of superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-α), and transforming growth factor-beta (TGF-β) and gene expressions of PI3K, pPI3K, AKT, and pAKT in renal tissue were detected. Renal histopathological and immunohistochemical studies were evaluated. DN + sitagliptin group showed significant decrease in FBG and kidney index, improvement in kidney function tests, and a decrease in levels of TNF-α and TGF-β in renal tissues compared with DN group. This was associated with significant increase in SOD and gene expressions of PI3K and AKT and their phosphorylated active forms in renal tissue in DN + sitagliptin group compared with DN group. Moreover, DN + sitagliptin group showed apparent decrease in amount of collagen fibers and expression of alpha-smooth muscle actin (α-SMA) compared with DN group. This work shows that sitagliptin improved renal functions and histopathological changes, impeded inflammation, and oxidative stress and upregulated PI3K/AKT pathway which highlights its renoprotective effects in a rat model of DN.

Icariin inhibits epithelial mesenchymal transition of renal tubular epithelial cells via regulating the miR-122-5p/FOXP2 axis in diabetic nephropathy rats

Epithelial mesenchymal transition (EMT) of renal tubular epithelial cells (RTECs) dominates the pathology of diabetic nephropathy (DN). microRNAs (miRNAs) can influence the fate of DN via regulation of EMT. This study aimed to analyze the role of Icariin (ICA) in EMT of RTECs, hoping to provide theoretical basis for DN management. The DN rat model was established using streptozocin, followed by ICA treatment, histopathological observation, and detection of creatinine and blood urea nitrogen. In vitro cell models were established using high glucose (HG), followed by assessment of cell proliferation, apoptosis, and migration, and E-cadherin, α-SMA, miR-122-5p, and FOXP2 expressions. Cells were transfected with miR-122-5p mimics or si-FOXP2 for joint experiments with ICA. The targeting relationship between miR-122-5p and FOXP2 was verified. ICA repaired renal dysfunctions and glomerular structure abnormities of DN rats in a dose-dependent manner. In vitro, ICA improved proliferation while suppressed migration, apoptosis, and EMT of RTECs. miR-122-5p was up-regulated in DN rats and suppressed by ICA, and miR-122-5p targeted FOXP2. miR-122-5p up-regulation or FOXP2 down-regulation reversed the protective effects of ICA on HG-induced RTECs. Overall, our finding ascertained that ICA inhibited miR-122-5p to promote FOXP2 transcription, thereby attenuating EMT of RTECs and renal injury in DN rats.

Nutraceuticals as a New Approach in Management of Diabetic Nephropathy

Diabetic nephropathy (DN), a fatal diabetic complication, is a prime reason of end-stage renal disease (ESRD), which is pathologically identified by thickened tubular basal and glomerular membranes, amassed extracellular matrix (ECM), and developing meningeal hypertrophy. Various deformities in the signaling pathway can interact to give rise to these pathologic activities in DN. In spite of the accessibility of numerous approaches to prevent these metabolic changes which include proper diet, exercising regularly, control of weight and control of drugs, epidemiological data are observing the growing tendency of the complication, indicating both the multifactorial nature of these disorders as well as the scarce conformance of patients to begin strategies. A number of Nutraceuticals utilized in clinical practice were shown to aim the pathophysiology of diabetes mellitus, metabolic disorder and their complications and to favorably modify numerous biochemical and clinical endpoints. These compounds comprise of antioxidants, vitamins like vitamin C, E, D; Omega 3 fatty acids, alpha lipoic acid (ALA), dietary fibers, flavonoids, phytoestrogens and minerals like chromium, magnesium. Various areas of concern prevail with regard of the use of nutraceuticals and dietary supplements in this setting, inclusive of standardization of products, potential side effects, definition of dosing regimen, interaction of drugs and need for evidence based interactions.