Kidney Antioxidant Research Articles

A Therapeutic Approach of Chitosan-loaded p-Coumaric Acid Nanoparticles to Alleviate Diabetic Nephropathy in Wister Rats.

This study evaluated the renoprotective effects of p-Coumaric acid nanoparticles (PCNPs) in nephropathic rats. Six groups of male Albino Wistar rats were randomly assigned. Group 1 was the control, while Group 2 received 45 mg/kg of streptozotocin (STZ) to induce diabetic nephropathy. Groups 3, 4, and 5 received STZ (45 mg/kg) along with PCNPs at doses of 20, 40, and 80 mg/kg, respectively. Group 6 received 80 mg/kg of PCNPs without STZ. Body weight, blood glucose, insulin, hemoglobin (Hb), and glycosylated hemoglobin (HbA1c) levels were measured. Blood urea, serum creatinine, kidney antioxidant enzymes, and lipid peroxidation levels were also analyzed. Histological and immunohistochemical studies of kidney tissues were performed. PCNPs (80 mg/kg) significantly reduced serum glucose, creatinine, and urea levels while increasing insulin levels and antioxidant activity in the kidneys. Histological analysis revealed that nephropathic rats exhibited cellular damage, including shrinkage of Bowman's capsule and lesions in the kidneys, along with degeneration in the Islets of Langerhans in the pancreas. PCNPs treatment restored these morphological alterations in the pancreas, liver, and kidneys to near-normal. Furthermore, nephropathic rats had elevated IL-6 and TNF-α expression in the renal tubules and glomeruli, which was reduced following PCNPs treatment. The findings suggest that PCNPs exhibit antihyperglycemic, antioxidant, antiglycation, and renoprotective effects in STZ-induced diabetic nephropathy.

The Effects of Acute Ammonia Nitrogen Stress on Antioxidant Ability, Phosphatases, and Related Gene Expression in the Kidney of Juvenile Yellowfin Tuna (Thunnus albacares)

This study investigated the effects of acute ammonia nitrogen (NH3-N) exposure on kidney antioxidant ability and phosphatases and related gene expression in juvenile yellowfin tuna (Thunnus albacares). The 180 juvenile yellowfin tuna (260.39 ± 55.99 g, 22.33 ± 2.28 cm) were exposed to ammonia for 6, 24, and 36 h using natural seawater (0 mg/L) as a control and NH3-N at 5 and 10 mg/L. The lipid peroxidation byproduct malondialdehyde (MDA) and the levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), alkaline phosphatase (AKP), and acid phosphatase (ACP), were measured using the colorimetric method in the trunk kidney to determine changes in antioxidant ability and phosphatase activity of juvenile yellowfin tuna exposed to NH3-N. Results indicated that, at 36 h, MDA, SOD, CAT, and GSH-PX levels rose in the 5 mg/L group versus the control. In the 10 mg/L group, MDA and SOD, CAT, and GSH-PX activities significantly increased after 24 and 36 h exposure compared to the control. Phosphatases play a pivotal role in the immune system. AKP activity significantly increased at 6 h, and ACP activity markedly rose at 36 h in the 5 mg/L group versus the control. Real-time fluorescence quantitative PCR was applied to detect alterations in the antioxidant genes SOD2, CAT, and glutathione peroxidase 1b (GPX1b) and immune cytokines-related genes Interleukin 10 (IL-10) and Interleukin 6 receptor (IL-6r) expression in the head kidney in juvenile tuna. Relative to the control, antioxidant gene expression in the 5 mg/L group significantly rose at 6 and 36 h, and in the 10 mg/L group, SOD2 and GPX1b were significantly elevated at 36 h. Compared to the control group, IL-10 expression in the 5 mg/L group significantly increased at 6 h, whereas IL-6r expression decreased. In the 10 mg/L group, both IL-10 and IL-6r levels were observed to be lower. Low ammonia nitrogen concentrations boost antioxidant defenses, phosphatase activities, and gene expression levels, whereas higher levels may induce suppressive effects. In yellowfin tuna juvenile farming, NH3-N concentration significantly affects the health of the juveniles. When the NH3-N concentration is between 5–10 mg/L, the stress duration should be limited to 24 h; if the concentration is below 5 mg/L, the stress duration can be extended to 36 h.

Modulatory role of Annona squamosa extract against streptozotocin-induced diabetic nephropathy in male rats

ABSTRACT Diabetic nephropathy (DN) is one of the most significant complications of diabetes mellitus. Annona squamosa has been demonstrated to have anti-inflammatory, anti-diabetic, and antioxidant properties. This study aimed to assess the modulatory role of A. squamosa fruit aqueous extract against DN. Forty male rats were divided into four groups: control group, A. squamosa extract (AE)-supplemented, diabetic (injected with a single dose of STZ), and diabetic + AE group. The diabetic rats treated with AE for four weeks revealed remarkable restoration in the levels of blood glucose and kidney functions disrupted by diabetes. These were manifested by significant improvement in the levels of urea, creatinine, and uric acid, as well as DN markers (β2 microglobulin, ceruloplasmin, NGAL, and plasma KIM-1). Additionally, the activity of lipid profiles (total cholesterol, triglycerides, LDH, and HDL), oxidative stress (MDA), and kidney antioxidants (CAT, SOD, GPx, and GSH) returned to normalcy. Also, the altered histological architecture of the kidney was markedly recovered after treatment with AE. Further, AE showed a proliferative and anti-inflammatory role, as indicated by modulation of PCNA and TNF-α expression in the kidney tissues. Annona squamosa extract significantly improved diabetic nephropathy in male rats via its antidiabetic, antioxidant and anti-inflammatory potential.

Protective effect of cinnamon extract against cobalt-induced multiple organ damage in rats.

The role of oxidative stress and inflammation in cobalt (Co) toxicity has been the focus of previous studies. Cinnamon and its main components have been reported to have protective effects in various tissues with antioxidant and anti-inflammatory effects. In this study, the protective effect of cinnamon extract (CE) against possible Co-induced heart, kidney, and liver damage in rats was investigated biochemically. Eighteen albino Wistar-type male rats were categorized into three groups (n = 6 per group): control (CG), CoCL2-administered (CoCL2), and CE + CoCL2-administered (CE + Co) groups. The CE + CoCL2 group was administered CE (100mg/kg), and the CoCL2 and CG groups were administered distilled water orally by gavage. One hour after the administration, Co (150mg/kg) was administered orally to the CE + CoCL2 and CoCL2 groups. This procedure was repeated once daily for 7days. Then, biochemical markers were studied in the excised heart, kidney, and liver tissues. CoCL2 increased oxidants and proinflammatory cytokines and decreased antioxidants in heart, kidney, and liver tissues. Heart, kidney, and liver tissue were affected by Co damage. CE treatment suppressed the CoCL2-induced increase in oxidants and proinflammatory cytokines and decrease in antioxidants in heart, kidney, and liver tissues. CE treatment has been shown to attenuate cardiac damage by reducing serum troponin I (TpI) and creatine kinase-MB (CK-MB), renal damage by reducing creatinine and blood urea nitrogen (BUN), and liver damage by reducing alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Co induced the production of oxidants and proinflammatory parameters and antioxidant depletion in heart, kidney, and liver tissues of rats. Our experimental results show that CE protects heart, kidney, and liver tissues against oxidative and inflammatory changes induced by CoCLl2.

Screening impacts of Tilmicosin-induced hepatic and renal toxicity in rats: protection by Rhodiola rosea extract through the involvement of oxidative stress, antioxidants, and inflammatory cytokines biomarkers.

Tilmicosin (TIL) is a semisynthetic macrolide antibiotic with a broad spectrum of activity derived from tylosin. TIL is effective in the treatment of bovine and ovine respiratory diseases caused by different microbes. In parallel, Rhodiola rosea (RHO) is a popular herbal remedy because of its anti-inflammatory and antioxidant qualities. The experiment lasted for 12days. Depending on the experimental group, the animals received either distilled water or RHO root extract dissolved in distilled water for 12days through a stomach tube, and the single subcutaneous injection on day 6 of the experiment of either 500 μL of 0.9% NaCl or TIL dissolved in 500 μL 0.9% NaCl. Samples and blood were collected for serum analysis, gene expression, and immunohistochemistry screening at liver and kidney levels. TIL injection increased serum levels of hepatic and renal markers (ALP, ALT, AST, TC, TG, creatinine, and urea) with decreased total proteins. In parallel, TIL induced hepatic and renal oxidative stress as there was an increase in malondialdehyde levels, with a decrease in catalase and reduced glutathione activities. Of interest, pre-administration of RHO inhibited TIL-induced increase in hepato-renal markers, decreased oxidative stress, and increased liver and kidney antioxidant activities. Quantitative RT-PCR showed that TIL increased the liver's HSP70 (heat shock protein), NFkB, and TNF-α mRNA expression. Moreover, TIL upregulated the expression of desmin, nestin, and vimentin expression in the kidney. The upregulated genes were decreased significantly in the protective group that received RHO. Serum inflammatory cytokines and genes of inflammatory markers were affected in liver tissues (HSP70, NFkB, and TNF-α) and kidney tissues (desmin, nestin, and vimentin)-TIL-induced hepatic vacuolation and congestion together with glomerular atrophy. The immunoreactivity of PCNA and HMGB1 was examined immunohistochemically. At cellular levels, PCNA was decreased while HMGB1 immunoreactivity was increased in TIL-injected rats, which was improved by pre-administration of RHO. RHO administration protected the altered changes in liver and renal histology. Current findings support the possible use of RHO to shield the liver and kidney from the negative effects of tilmicosin.

Effects of Buccholzia coriacea (wonderful kola) on hepatoprotective, nephrotective and oxidative stress of aluminium chloride induced wistar rats

Buchholzia coriacea seeds has been reported to have various medicinal properties. This study evaluates the effect of the aqueous extract of Buchholzia coriacea seed (wonderful kola), on Aluminium chloride induced liver toxicity in adult male Wistar rats. 24 rats weighing between 150 g - 210 g were divided into five groups. Group A- (the control group) received water and animal chow. Group B received 200mg/kg of AlCl3 only, Group C received aluminum chloride and vitamin C for 14 days. Group D received 250 mg/kg body weight body weight (Low Dose) of aqueous extract Buchholzia coriacea and (200 mg/kg) AlCl3. Group E received 1000mg/kg body weight (High Dose) of aqueous extract of Buchholziacoriacea and (250mg/kg) AlCl3. The animals were sacrificed, the liver and kidney was excised and processed for routine paraffin sections at 5micromes thick. Sections were stained with Haematoxylin and Eosin to demonstrate histoarchitecture. Biochemical analysis was also carried out to determine the effects on liver and kidney antioxidant enzymes. Histological assessment showed narrowed central vein, degeneration of hepatocytes and distortion of sinusoids in the AlCl3 alone treated groups. The histoarchitecture of the liver in the other groups showed improvement especially in Group E (High Dose of B. coriacea) and Group C (vitamin C and aluminum chloride only). The biochemical analysis on the other hand showed significantly reduced activities in GSH, SOD, CAT and significantly increased level of MDA in the AlCl3 only group. In the other groups, MDA levels reduced, GSH, SOD and CAT also increased enzymatic activities following the administration of B. coriacea. The study concludes that Buchholziacoriacea seed extract plays a role in protecting liver and kidney from AlCl3 toxicity.

Water-soluble phenolics from Phoenix dactylifera fruits as potential reno-protective agent against cisplatin-induced toxicity: pre- and post-treatment strategies

Nephrotoxicity is the major side effect of cisplatin, an effective platinum-based chemotherapeutic drug that is applicable in the treatment of several solid-tissue cancers. Studies have indicated that certain water-soluble phenolics offer renal protection. Thus, this study investigates the role of pre and post-treatment of rats with water-soluble phenolics from Phoenix dactylifera (PdP) against nephrotoxicity induced by cisplatin. Rats were either orally pretreated or post-treated with 200 mg/kg body weight of PdP before or after exposure to a single therapeutic dose of cisplatin (5 mg/kg body weight) for 7 successive days intraperitoneally. The protective effects of PdP against Cisplatin-induced nephrotoxicity was based on the evaluation of various biochemical and redox biomarkers, together with histopathological examination of kidney tissues. The composition, structural features, and antioxidative influence of PdP were determined based on chromatographic, spectroscopic, and in vitro antioxidative models. Cisplatin single exposure led to a substantial increase in the tested renal function biomarkers (uric acid, creatinine, and urea levels), associated with an increase in malondialdehyde indicating lipid peroxidation and a significant decline (p < 0.05) in reduced glutathione (GSH) levels in the renal tissue when compared with the control group. A marked decline exists in the kidney antioxidant enzymes (catalase, SOD, and GPx). Nevertheless, treatment with PdP significantly suppressed the heightened renal function markers, lipid peroxidation, and oxidative stress. Spectroscopic analysis revealed significant medicinal phenolics, and in vitro tests demonstrated antioxidative properties. Taken together, results from this study indicate that pre- and/or post-treatment strategies of PdP could serve therapeutic purposes in cisplatin-induced renal damage.

Hematological changes, oxidative stress assessment, and dysregulation of aquaporin-3 channel, prolactin, and oxytocin receptors in kidneys of lactating Wistar rats treated with monosodium glutamate.

High consumption of locally produced delicacies could expose nursing mothers to high monosodium glutamate (MSG) levels, frequently used as a necessary condiment in low-income countries. Thus, this study evaluated some novel preliminary changes in renal hormonal receptors, the aquaporin-3 channel, oxidative stress markers, and hematological indices induced by monosodium glutamate in lactating rats. Post-parturition, twenty-four (24) lactating Wistar rats were divided into four (4) groups of six rats each (n = 6). Oral administration of distilled water and MSG started three (3) days postpartum as follows: group 1: distilled water (1ml/kg BW), group 2: MSG (925mg/kg BW), group 3: MSG (1850mg/kg BW), and group 4: MSG (3700mg/kg BW). At the end of the experiment, which lasted fourteen (14) days, animals were sacrificed and samples of blood and tissues were obtained for biochemical analysis. MSG administration significantly (p < 0.05) increased ROS and MDA, with a significant (p < 0.05) decrease in kidney antioxidants. Serum creatinine, total, conjugated, and unconjugated bilirubin significantly (p < 0.05) increased with MSG administration. The prolactin receptor was significantly reduced (p < 0.05), while the oxytocin receptor and aquaporin-3 channel were significantly (p < 0.05) increased in the MSG-administered groups. There were significant (p < 0.05) changes in the hematological indices of the MSG-administered animals. Thus, the findings of this study suggest that high MSG consumption causes hematological alterations and may alter renal function via increased ROS production and dysregulation of the AQP-3 channel, prolactin, and oxytocin receptors in the kidneys of lactating Wistar rats.

Renoprotective Effect of Pitavastatin against TAA-Induced Renal Injury: Involvement of the miR-93/PTEN/AKT/mTOR Pathway.

This research investigated if pitavastatin (Pita) might protect rats' kidneys against thioacetamide (TAA). By altering the PTEN/AKT/mTOR pathway, pitavastatin may boost kidney antioxidant capacity and minimize oxidative damage. Statins have several benefits, including antioxidant and anti-inflammatory characteristics. The principal hypothesis of this study was that Pita can regulate the miR-93/PTEN/AKT/mTOR pathways, which is thought to be responsible for its renoprotective effects. The experiment divided male rats into four groups. Group 1 included untreated rats as the control. Group 2 included rats which received TAA (100 mg/kg intraperitoneally thrice a week for two weeks) to destroy their kidneys. Groups 3 and 4 included rats which received Pita orally at 0.4 and 0.8 mg/kg for 14 days after TAA injections. Renal injury increased BUN, creatinine, and MDA levels and decreased glutathione (GSH) levels. Pitavastatin prevented these alterations. TAA decreased PTEN and increased miR-93, Akt, p-Akt, mTOR, and Stat3 in the kidneys. Pitavastatin also regulated the associated culprit pathway, miR-93/PTEN/Akt/mTOR. In addition, TAA induced adverse effects on the kidney tissue, which were significantly ameliorated by pitavastatin treatment. The findings suggest that pitavastatin can attenuate renal injury, likely by regulating the miR-93/PTEN/Akt/mTOR pathway. This modulation of the pathway appears to contribute to the protective effects of pitavastatin against TAA-induced renal injury, adding to the growing evidence of the pleiotropic benefits of statins in renal health.

Reduced Progression of Diabetic Nephropathy in Streptozocin-Induced Diabetic rats by Lannea coromandelica Leaf Extract

Objectives: An important contributor to end-stage renal failure globally is diabetic kidney disease. The current study looked at the safeguarding results of an infusion of Ethanol from Lannea coromandelica houtt leaves (ELCL)in diabetic kidney disease that was caused by streptozotocin with the intention to treat diabetic nephropathy, creating supportive and substitute medicine is necessary. The development of DN may be slowed down by itsanti-inflammatory, anti-diabetic and antioxidant qualities. The novelity lies in the plant selection for the study. Methods: Streptozotocin (45mg/kg, i.p.) was administered as a single dosage to rats to induce diabetes. During 8 weeks, oral dosages of ELCL (100mg/kg and 200mg/kg.) were given to rodents with STZ diabetes. Blood sugar amounts and body and kidney weights were measured at the conclusion of the trial period. The parameters of serum and urine were evaluated. The kidney levels of lipid peroxide and antioxidant enzymes were assessed. Results: In STZ-diabetic rats and rats treated with extract, ethylacetate extract dramatically raised body weight and decreased blood glucose, blood urea levels, blood nitrogen levels, and the creatinine levels. All kidney antioxidants, including glutathione synthetase, glutathione-S-transferase, catalase, superoxide dismutase and NAD(P) H dehydrogenase [quinone]1 were highly upregulated by the extract. Conclusion: According to research, ELCL may have antioxidant, antihyperglycemic, and anti-glycation properties that could slow the progression of diabetic nephropathy.

Paris polyphylla Sm. extract enriched with diosgenin as an antidiabetic agent: In vitro and in vivo study

BackgroundThe global epidemic of diabetes mellitus (DM) has become a severe metabolic disorder and a threat to public health. Medicinal plants as a remedy for managing diabetes is accepted worldwide due to their long-term effectiveness and fewer side effects, mainly attributed to the phytochemicals. Paris polyphylla is a valuable medicinal herb endowed with steroidal saponins of therapeutic importance. The plant is popularly used as an anticancer agent. However, the antidiabetic potential of P. polyphylla has not been explored. So, the present study was undertaken to investigate the antidiabetic potential of P. polyphylla extract enriched with diosgenin (PPED) in vitro and in vivo in streptozotocin (STZ) induced diabetic rats. MethodP. polyphylla rhizomes were used to extract diosgenin-enriched extracts. The P. polyphylla extract enriched with diosgenin (PPED) was quantified using standard diosgenin in HPLC. The in vitro antidiabetic efficacy of PPED was determined by α-glucosidase and α-amylase enzyme inhibitory activity. PPED 1 (200 mg/kg b.w) and PPED 2 (400 mg/kg b.w) was administered in normal glycemic rats to evaluate the oral glucose tolerance test (OGTT). PPED 1 and PPED 2 were orally dosed for 28 days daily in STZ-induced diabetic rats, and the fasting blood glucose level and body weight were monitored every 7 days. Furthermore, the antioxidant, serum biochemical parameters, and pancreatic histopathology were studied. ResultsP. polyphylla extract enriched with diosgenin was quantified. PPED exhibited a concentration-dependent inhibition of α-amylase and α-glucosidase enzymes with IC50 275.7 ± 0.59 μg/mL and 121.9 ± 1.21 μg/mL. Daily oral dosage of PPED 1 and PPED 2 for 28 days leads to a significant decrease in fasting blood glucose level and recovery of body weight compared to the diabetic control. The liver and kidney antioxidant parameters also improved with PPED dosage. According to our study, the PPED 1 and PPED 2 treated groups showed a decrease in glycated hemoglobin (HbA1c) and hyperlipidemia, as well as an improvement in protein, liver, and kidney function parameters. Moreover, PPED administration also ameliorates the pancreatic islets' size and β-cell granularity compared to the diabetic control group. It is, therefore, possible to conclude that PPED has the potential as an antidiabetic agent. ConclusionThis is the first report of P. polyphylla extract enriched with diosgenin as a potent antidiabetic agent. The present study broadens the therapeutic horizon of P. polyphylla as an invaluable medicinal plant.

LC/MS-Based Profiling of Hedyotis aspera Whole-Plant Methanolic Extract and Evaluation of Its Nephroprotective Potential against Gentamicin-Induced Nephrotoxicity in Rats Supported by In Silico Studies

Many high-altitude plants, such as Hedyotis aspera, need to be explored for their possible medicinal value. The current study explored the protective effect of Hedyotis aspera methanolic extract whole plant (HAME) against gentamicin-induced nephrotoxicity in rats. It profiled their phytocontents using HPLC-QTOF-MS/MS analytic methods. The LC-MS analysis of HAME revealed 27 compounds. Eight compounds followed Lipinski’s rule of five and were found to be potential TNF-α inhibitors with binding affinities of −6.9, −6.3, −6.3, and −6.3 Kcal/mol, such as 14,19-Dihydroaspidospermatine, coumeroic acid, lycocernuine and muzanzagenin. All potential compounds were found to be safe according to the ADMET analysis. The in vitro 2,2-diphenyl-1-picrlhydrazyl (DPPH) assay assessed the antioxidant activity. The nephroprotective activity was assessed in rats using a gentamicin-induced nephrotoxicity model. The in vivo analysis involved histological examination, tissue biochemical evaluation, including a kidney function test, catalase activity (CAT), reduced glutathione (GSH) levels, superoxide dismutase (SOD), and the inflammatory mediator TNF-α. Based on DPPH activity, HAME showed a scavenging activity IC50 of 264.8 ± 1.2 µg/mL, while results were compared with a standard vitamin C IC50 of 45 ± 0.45 µg/mL. Nephrotoxicity was successfully induced, as shown by elevated creatinine and uric acid levels, decreased kidney antioxidant levels, and increased TNF-α in gentamicin-treated rats. The HAME treatment significantly reduced serum creatinine and uric acid levels, increased GSH (p &lt; 0.01 **), CAT (p &lt; 0.01 **), and SOD (p &lt; 0.001 ***), and decreased TNF-α (p &lt; 0.001 ***) in nephrotoxic rats. The histopathological examination of the groups treated with HAME revealed a notable enhancement in the structural integrity of the kidneys as compared to the group exposed to gentamicin. Biochemical, histopathological, and phytochemical screening of HAME suggests that it has nephroprotective potential, owing to the presence of 14,19-Dihydroaspidospermatine, coumeroic acid, lycopene, and muzanzagenin.

Ageratina adenophora (Spreng.) King & H. Rob. Standardized leaf extract as an antidiabetic agent for type 2 diabetes: An in vitro and in vivo evaluation.

Type 2 diabetes has become one of the major health concerns of the 21st century, marked by hyperglycemia or glycosuria, and is associated with the development of several secondary health complications. Due to the fact that chemically synthesized drugs lead to several inevitable side effects, new antidiabetic medications from plants have gained substantial attention. Thus, the current study aims to evaluate the antidiabetic capacity of the Ageratina adenophora hydroalcoholic (AAHY) extract in streptozotocin-nicotinamide (STZ-NA)-induced diabetic Wistar albino rats. The rats were segregated randomly into five groups with six rats each. Group I was normal control, and the other four groups were STZ-NA-induced. Group II was designated diabetic control, and group III, IV, and V received metformin (150mg/kg b.w.) and AAHY extract (200 and 400mg/kg b.w.) for 28days. Fasting blood glucose, serum biochemicals, liver and kidney antioxidant parameters, and pancreatic histopathology were observed after the experimental design. The study concludes that the AAHY extract has a significant blood glucose lowering capacity on normoglycemic (87.01 ± 0.54 to 57.21 ± 0.31), diabetic (324 ± 2.94 to 93 ± 2.04), and oral glucose-loaded (117.75 ± 3.35 to 92.75 ± 2.09) Wistar albino rats. The in vitro studies show that the AAHY extract has α-glucosidase and α-amylase inhibitory activities which can restore the altered blood glucose level, glycated hemoglobin, body weight, and serum enzymes such as serum glutamic pyruvic transaminase, serum glutamic oxaloacetic transaminase, serum alkaline phosphatase, total protein, urea, and creatinine levels close to the normal range in the treated STZ-NA-induced diabetic rats. The evaluation of these serum biochemicals is crucial for monitoring the diabetic condition. The AAHY extract has significantly enhanced tissue antioxidant parameters, such as superoxide dismutase, glutathione, and lipid peroxidation, close to normal levels. The presence of high-quantity chlorogenic (6.47% w/w) and caffeic (3.28% w/w) acids as some of the major phytoconstituents may contribute to the improvement of insulin resistance and oxidative stress. The study provides scientific support for the utilization of A. adenophora to treat type 2 diabetes in the STZ-NA-induced diabetic rat model. Although the preventive role of the AAHY extract in treating Wistar albino rat models against type 2 diabetes mellitus is undeniable, further elaborative research is required for efficacy and safety assessment in human beings.

Chemical characterization of Hymenocardia acida stem bark extract and modulation of selected enzymes in Kidney and Heart of Wistar rats

Hymenocardia acida tul leaf and stem bark are used in treatment of several diseases in Africa. We examined the chemical constituents of the stem bark extract and its effects on some antioxidant indices and esterases in Wistar rats. Hymenocardia acida stem bark extract (HASBE) was obtained by Soxhlet extraction using methanol, followed by Atomic Absorption Spectroscopy (AAS), Fourier-Transform Infrared (FT-IR) spectroscopy, ultraviolet (UV) spectroscopy, High-performance liquid chromatography (HPLC) and Gas Chromatography-Flame ionization detection (GC-FID). Forty-eight male Wistar rats were assigned into eight groups (6 rats each), and administered orally with normal saline (Control), 50, 100, 150, 200, 250, 300, 350 mg/kg of HASBE twice per week for eight weeks. The rats were sacrificed under chloroform anesthesia, and kidneys and heart were excised, and processed into homogenates. Superoxide dismutase (SOD), catalase, lipid peroxidation (LPO), glutathione peroxidase (GPx), acetylcholinesterase (AChE) and carboxylesterases (CES) were determined spectrophotometrically. The AAS of HASBE detected Cobalt, Copper, Zinc, Iron, Nickel, Chromium, Manganese and Magnesium. The FT-IR shows four peaks as 2961.4, 2926.0, 1056.7 and 1034.3 cm-1, while UV shows absorbance between 250 nm and 650 nm. The HPLC identified orientin, β-sitosterol, rutin and betulinic acid, while GC-FID identified rutin, orientin, stigmasterol, hymenocardine and homopterocarpin as prominent compounds. The SOD significantly (p &lt; 0.05) reduced in kidneys, while catalase was elevated in kidney and heart, with an increase in LPO level only in heart, relative to controls. The GPx, AChE and CE activities in kidneys were increased by HASBE, whereas, CE activity was lowered in heart. This study has demonstrated that Hymenocardia acida stem bark extract majorly contains iron, nickel, orientin, rutin, stigmasterol, hymenocardine, β-sitosterol, homopterocarpin and betulinic acid, and could possibly modulate the activities of antioxidant and esterase enzymes in kidney and heart of Wistar rats.

Effects of Water Temperature on the Growth, Antioxidant Capacity, and Gut Microbiota of Percocypris pingi Juveniles

It is necessary to determine the optimal temperature for Percocypris pingi growth in recirculating aquaculture systems. To describe the effects of temperature, we evaluated the growth, antioxidant enzyme activity, and gut microbiota structure of P. pingi at different temperatures, including 14, 18, 22, and 26 °C. Results showed that increases in body weight of individuals of the groups subjected to 18 and 22 °C temperatures were considerably higher than those in the groups subjected to temperatures of 14 and 26 °C between 20 and 60 d after the experiment started. Acid phosphatase activity in the liver and kidneys of P. pingi did not differ significantly among the various temperature groups (p &gt; 0.05). A gradual restoration of the alkaline phosphatase and superoxide dismutase activities to variations in the surrounding temperature was observed in the liver and kidney of P. pingi. Interestingly, the water temperature did not affect the α-diversity or composition of the gut microbiota of P. pingi. In conclusion, water temperatures between 14 and 26 °C significantly impacted the growth of P. pingi (p &lt; 0.05) but not the liver and kidney antioxidant capacity or the gut microbiota within 60 d.

Isolation, Characterization, Antioxidant, and Wound Healing Activities of Extracellular Polysaccharide from Endophytic Fungus Talaromyces purpureogenus.

In this study, two extracellular polysaccharides (TEPS1 and TEPS2) were isolatedfrom the endophytic fungus (Talaromyces purpureogenus) and purified by DEAE-Sepharose Fast Flow column using NaCl as gradient eluent. The HPLC analysis displayed that TEPS1 was composed of mannose (38.70%), ribose (25.02%), glucose (19.34%), and galactose (16.94%) while the TEPS2 composed by mannose (100%). The NMR results indicated that TEPS1 exhibited α-glycosidic configurations. The both polysaccharides, TEPS1 and TEPS2 were exhibited a good antioxidant activity interms of DPPH, ABTS, and •OH scavenging. However, TEPS1 showed a higher antioxidant activity than TEPS2. The IC50 of TEPS1 were 32.16, 192.57, and 54.67μg·mL-1, for DPPH, ABTS, and •OH radicalscavenging, respectively. Furthermore, TEPS1 showed the high cellular antioxidant and wound healing activity in the human embryonic kidney (HEK293) cell line. Overall, these two polysaccharides were promising inantioxidant activity.

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.

Abietic acid ameliorates nephropathy progression via mitigating renal oxidative stress, inflammation, fibrosis and apoptosis in high fat diet and low dose streptozotocin-induced diabetic rats

BackgroundAbietic acid (AA) has been reported to exhibit anti-inflammatory activity, however its protective effect against inflammation and its trigger factor i.e., oxidative stress and the related sequelae i.e., apoptosis and fibrosis in the kidney in diabetes mellitus (DM) is unknown. PurposeTo identify the ability of AA to mitigate the inflammatory and inflammation-related insults to the kidney in DM. Methods & Study designAdult male rats were induced type-2 DM by feeding with a high-fat diet for twelve weeks followed by injection with a single dose of streptozotocin (STZ) (30 mg/kg/bw) intraperitoneally at twelve weeks. Following DM confirmation, AA (10 and 20 mg/kg/day) was given orally for another four weeks. Then the fasting blood glucose (FBG) and renal profile were determined and oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) tests were performed. A day after the last treatment, rats were sacrificed and kidneys were harvested and subjected for histopathological and molecular biological analysis. ResultsAA treatment was found to reduce the FBG, serum urea and creatinine levels (p < 0.05) while improving the OGTT and ITT (p < 0.05) in diabetic rats. Besides, AA treatment also mitigated kidney histopathological changes, reduces kidney oxidative stress as reflected by reduced levels of RAGE and Keap1 but increased levels of kidney antioxidants Nrf2, SOD, CAT, GPX, HO-1 & NQO-1 (p < 0.05). Additionally, AA treatment also decreases kidney inflammation (NF-kB p65, IL-1β, IL-6, TNF-α and iNOS) and fibrosis (TGF-β1 and GSK-3β) (p < 0/05). Kidney apoptosis decreased as reflected by decreased levels of Bax, caspase-3 and caspase-9 while its anti-apoptosis Bcl-2 protein levels increased (p < 0.05). ConclusionAA helps to mitigate nephropathy development in DM via counteracting oxidative stress, inflammation and apoptosis.

Chemopreventive effects of hesperidin against paclitaxel-induced hepatotoxicity and nephrotoxicity via amendment of Nrf2/HO-1 and caspase-3/Bax/Bcl-2 signaling pathways

Paclitaxel (PTX) is a widely used chemotherapeutic drug particularly effective against lung, breast, and ovarian cancer, though its usefulness is limited due to its multi-organ toxicity. The mechanisms underlying PTX toxicity are currently not yet known and there are no approved treatments for its control or prevention. This study aimed to investigate whether hesperidin (HSP) had a protective effect on paclitaxel-induced hepatotoxicity and nephrotoxicity from biochemical, and molecular perspectives. The rats were administered PTX 2 mg/kg, b.w. intraperitoneally for the first 5 consecutive days, then 100 or 200 mg/kg b.w. HSP orally for 10 consecutive days. Our results demonstrated that HSP decreased the PTX induced lipid peroxidation, improved the serum hepatic and renal functions (by decreasing the levels of AST, ALT, ALP, urea, and creatinine), and restored the liver and kidney antioxidant armory (SOD, CAT, GPx, and GSH). HSP also significantly reduced mRNA expression levels of NF-κB, TNF-α, IL-1β, IL-6, MAPK 14, Caspase-3, Bax, LC3A, LC3B, MMP2, and MMP9 whereas caused an increase in levels of Nrf2, HO-1, and Bcl-2 in the kidney and liver of PTX-induced rats. In addition, caspase-3, Bax, and Bcl-2 protein levels were examined by Western blot analysis, and it was determined that HSP decreased caspase-3 and Bax protein levels, but increased Bcl-2 protein levels. The findings of the study suggest that HSP has chemopreventive potential against PTX-induced hepatorenal toxicity plausibly through the attenuation of oxidative stress, inflammation, apoptosis, and autophagy.

Exosomes Derived from BM-MSCs Mitigate the Development of Chronic Kidney Damage Post-Menopause via Interfering with Fibrosis and Apoptosis.

The rate of chronic kidney disease (CKD) is increasing globally, and it is caused by continuous damage to kidney tissue. With time the renal damage becomes irreversible, leading to CKD development. In females, post-menopause lack of estrogen supply has been described as a risk factor for CKD development, and studies targeting post-menopause CKD are scarce. In the present study, we used exosomes isolated from bone marrow mesenchymal stem/stromal cells (BM-MSCs) to test their therapeutic potential against the development of CKD. At first, the menopause model was achieved by surgical bilateral ovariectomy in female albino rats. After that, 100 µg of exosomes was given to ovariectomized rats, and the study continued for 2 months. Changes in urine volume, urine protein content, kidney function biochemical parameters (creatinine and BUN), kidney antioxidant parameters (SOD, GPx and CAT), histological changes, immunohistochemical levels of caspase 3, and the gene expression of NGAL (related to kidney damage), TGFβ1 and αSMA (related to fibrosis and EMT), and caspase 3 (related to apoptosis) were studied. After the ovariectomy, the occurrence of CKD was confirmed in the rats by the drastic reduction of serum estrogen and progesterone levels, reduced urine output, increased urinary protein excretion, elevated serum creatinine and BUN, reduced GPx SOD, and CAT in kidney tissue, degenerative and fibrotic lesions in the histopathological examination, higher immunohistochemical expression of caspase 3 and increased expression of all studied genes. After exosomes administration, the entire chronic inflammatory picture in the kidney was corrected, and a near-normal kidney structure and function were attained. This study shows for the first time that BM-MSCs exosomes are potent for reducing apoptosis and fibrosis levels and, thus, can reduce the chronic damage of the kidneys in females that are in their menopause period. Therefore, MSCs-derived exosomes should be considered a valuable therapy for preserving postmenopausal kidney structure and function and, subsequently, could improve the quality of females’ life during menopause.