s-Ethyl cysteine, an amino acid derivative, attenuated cisplatin induced nephrotoxicity.

Renal protection from s-ethyl cysteine (SEC) against cisplatin (CP)-induced inflammatory and oxidative injury was examined. Mice were divided into five groups: normal group, 0.25% SEC group, CP group, 0.125% SEC + CP group, 0.25% SEC + CP group. After 2 weeks supplementation, mice of CP and SEC + CP groups received CP treatment. H&E stain showed that CP caused infiltration of inflammatory cells and necrosis of tubular cells. SEC pre-treatments attenuated CP-induced inflammatory injury and degeneration. SEC pre-treatments limited CP-stimulated release of interleukin (IL)-1beta, IL-6, tumor necrosis factor-alpha and prostaglandin E2 in kidney. CP raised the renal activity and mRNA expression of cyclooxygenase-2 and nuclear factor kappa B. SEC pre-treatments reversed these alterations. CP increased the production of reactive oxygen species and nitric oxide, and lowered glutathione content, glutathione peroxidase and glutathione reductase activities in kidney. SEC pre-treatments reversed these changes. CP up-regulated renal inducible nitric oxide synthase (iNOS) mRNA expression, and down-regulated nuclear factor E2-related factor (Nrf)-2 and heme oxygenase (HO)-1 mRNA expression. SEC pre-treatments suppressed iNOS mRNA expression; and enhanced renal Nrf2 and HO-1 mRNA expression. These novel findings suggest that dietary SEC via exerting its multiple bio-functions could be considered as a protective agent for kidney against CP.

Greater Protective Potent of s-Methyl Cysteine and Syringic Acid Combination for NGF-differentiated PC12 Cells against Kainic acid-induced Injury.

Objective: The effects of pre-treatments from s-methyl cysteine (SMC) alone, syringic acid (SA) alone and SMC plus SA against kainic acid (KA) induced injury in nerve growth factor (NGF) differentiated PC12 cells were investigated. Methods: NGF-differentiated PC12 cells were treated with 1 µM SMC, 1 µM SA or 0.5 µM SMC plus 0.5 µM SA for 2 days. Subsequently, cells were further treated by 150 µM KA. Results: KA suppressed Bcl-2 mRNA expression, enhanced Bax mRNA expression and casued cell death. SMC was greater than SA, and similar as SMC+SA in increasing Bcl-2 mRNA expression. SMC+SA led to greater increase in mitochondrial membrane potential and cell survival than SMC or SA alone. SMC+SA resulted in more reduction in reactive oxygen species and tumor necrosis factor-alpha generation, more increase in glutathione content and glutathione reductase activity than SMC or SA alone. KA up-regulated protein expression of nuclear factor kappa B (NF-κB) p65 and phosphorylated p38 (p-p38). SMC or SA pre-treatments alone limited protein expression of both factors. SMC+SA resulted in more suppression in NF-κB p65 and p-p38 expression. KA decreased glutamine level, increased glutamate level and stimulated calcium release. SMC pre-treatments alone reversed these alterations. SMC alone elevated glutamine synthetase (GS) activity and mRNA expression. SMC+SA led to greater GS activity and mRNA expression than SMC pre-treatments alone. Conclusion: These findings suggested that this combination, SMC+SA, might provide greater protective potent for neuronal cells.

Cantharidin decreased viable cell number in human osteosarcoma U-2 OS cells through G2/M phase arrest and induction of cell apoptosis.

Cantharidin (CTD), a sesquiterpenoid bioactive substance, has been reported to exhibit anticancer activity against various types of cancer cells. The aim of the present study was to investigate the apoptosis effects and the underlying mechanisms of CTD on osteosarcoma U-2 OS cells. Results showed that CTD induced cell morphologic changes, reduced total viable cells, induced DNA damage, and G2/M phase arrest. CTD increased the production of reactive oxygen species and Ca2+, and elevated the activities of caspase-3 and -9, but decreased the level of mitochondrial membrane potential. Furthermore, CTD increased the ROS- and ER stress-associated protein expressions and increased the levels of pro-apoptosis-associated proteins, but decreased that of anti-apoptosis-associated proteins. Based on these observations, we suggested that CTD decreased cell number through G2/M phase arrest and the induction of cell apoptosis in U-2 OS cells and CTD could be a potential candidate for osteosarcoma treatments.

Pteris multifida, Cortex phellodendri, and probiotics attenuated inflammatory status and immunity in mice with a Salmonella enterica serovar Typhimurium infection.

Pteris multifida (PM) and Cortex phellodendri (CP) are medicinal foods used for gastrointestinal protection. Lactic-acid bacteria are probiotics. Salmonella Typhimurium strain ST21-infected mice were used to examine the alleviative effects of two lactic-acid bacteria (LAB) as well as aqueous extracts of PM and CP for a 4-day treatment. CP and LAB decreased fecal ST counts. CP and PM reduced the ST21 count in the blood, intestine, and liver. LAB lowered the ST21 count in the intestine and spleen. CP and LAB decreased the IFN-gamma level; PM lowered the TNF-alpha level; and both LAB and PM reduced the IL-1beta level in serum. PM and CP lowered the IgG level in serum. The data in a macrophage infection model indicate that TNF-alpha was partial involved in this alleviative effects, other mechanisms might be involved. In sum, these novel findings suggest that PM, CP, and LAB probiotics are potential anti-Salmonellae agents.

Houttuynia cordata aqueous extract attenuated glycative and oxidative stress in heart and kidney of diabetic mice.

PURPOSE: The anti-glycative and anti-oxidative effects from Houttuynia cordata leaves aqueous extract (HCAE) in heart and kidney of diabetic mice were examined. METHODS: HCAE, at 1 or 2 %, was supplied in drinking water for 8 weeks. Plasma glucose and blood urea nitrogen (BUN) levels and creatine phosphokinase (CPK) activity were measured. The production of oxidative and inflammatory factors was determined. Activity and protein expression of associated enzymes or regulators were analyzed. RESULTS: HCAE intake at both doses lowered plasma glucose and BUN levels, and CPK activity and also restored creatinine clearance rate in diabetic mice. HCAE intake, only at 2 %, retained plasma insulin levels (P < 0.05). HCAE reduced reactive oxygen species, protein carbonyl, interleukin-6, tumor necrosis factor-alpha, N (ε) -(carboxymethyl)-lysine, pentosidine and fructose levels, and reserved glutathione content in heart and kidney of diabetic mice (P < 0.05). Diabetes enhanced aldose reductase (AR) activity and protein expression in heart and kidney (P < 0.05). HCAE intake at both doses decreased renal AR activity and protein expression, but only at 2 % lowered cardiac AR activity and protein expression (P < 0.05). Diabetes increased protein expression of RAGE, p47(phox) and gp91(phox), nuclear factor kappa-B (NF-κB) p50, NF-κB p65 and mitogen-activated protein kinase in heart and kidney (P < 0.05). HCAE intake only at 2 % limited RAGE expression, but at 1 and 2 % downregulated p47(phox), NF-κB p65 and p-p38 expression in these organs (P < 0.05). CONCLUSIONS: These findings suggest that Houttuynia cordata leaves aqueous extract could ameliorate cardiac and renal injury under diabetic condition.

Advanced Glycation End-Products Enhance Lung Cancer Cell Invasion and Migration.

Effects of carboxymethyllysine (CML) and pentosidine, two advanced glycation end-products (AGEs), upon invasion and migration in A549 and Calu-6 cells, two non-small cell lung cancer (NSCLC) cell lines were examined. CML or pentosidine at 1, 2, 4, 8 or 16 µmol/L were added into cells. Proliferation, invasion and migration were measured. CML or pentosidine at 4-16 µmol/L promoted invasion and migration in both cell lines, and increased the production of reactive oxygen species, tumor necrosis factor-α, interleukin-6 and transforming growth factor-ß1. CML or pentosidine at 2-16 µmol/L up-regulated the protein expression of AGE receptor, p47(phox), intercellular adhesion molecule-1 and fibronectin in test NSCLC cells. Matrix metalloproteinase-2 protein expression in A549 and Calu-6 cells was increased by CML or pentosidine at 4-16 µmol/L. These two AGEs at 2-16 µmol/L enhanced nuclear factor κ-B (NF-κ B) p65 protein expression and p38 phosphorylation in A549 cells. However, CML or pentosidine at 4-16 µmol/L up-regulated NF-κB p65 and p-p38 protein expression in Calu-6 cells. These findings suggest that CML and pentosidine, by promoting the invasion, migration and production of associated factors, benefit NSCLC metastasis.

Protective Effects of Red Guava on Inflammation and Oxidative Stress in Streptozotocin-Induced Diabetic Mice.

Diabetes is an important chronic disease and the 4th leading cause of death in Taiwan. Hyperglycemia-induced oxidative and inflammatory damage are the main causes of chronic complications in diabetic patients. The red guava (red-fleshed guava cultivar of Psidium guajava L.) is a tropical fruit belonging to the Myrtaceae family and an important commercial crop in Taiwan. In this study, the protective effects of a diet containing red guava on inflammation and oxidative stress in streptozotocin (STZ)-induced diabetic mice were examined. The experimental group was divided into seven subgroups: normal (N), diabetes mellitus (DM), diabetes + red guava 1% (L), 2% (M), and 5% (H), diabetes + 5% red guava + anti-diabetic rosiglitazone (HR), and diabetes + anti-diabetic rosiglitazone (R). The mice were fed for 8 weeks and sacrificed by decapitation. Compared with the DM group, the experimental groups with diets containing red guava as well as rosiglitazone all showed significant improvements in blood glucose control, insulin resistance, creatinine, blood urea nitrogen, triglycerides, non-esterified fatty acids, cholesterol, c-reactive protein, TNF-α, and IL-10. Furthermore, the expression of inflammatory proteins, such as iNOS and NF-κB, was suppressed via activated PPARγ, and the expression levels of GPx3 and ACO increased. In summary, red guava can significantly suppress inflammatory and oxidative damage caused by diabetes and alleviate diabetic symptoms; thus, it exerts protective effects and has potential applications for the development of a dietary supplement.

Phytochemical profile, antioxidative and anti-inflammatory potentials of Gynura bicolor DC.

BACKGROUND: The phytochemical composition of aqueous and ethanol extracts from Gynura bicolor DC., a vegetable, was determined. Human umbilical vein endothelial (HUVE) cells were used to examine the antioxidative and anti-inflammatory potentials of these extracts at 1, 2 or 4% (v/v) against high-glucose-induced injury. RESULTS: Both aqueous and ethanol extracts contained phenolic acids, flavonoids, carotenoids and anthocyanins in the ranges 1428-1569, 1934-2175, 921-1007 and 2135-2407 mg per 100 g dry weight respectively. Both extracts were rich in quercetin, lutein, malvidin and pelargonidin. Addition of these extracts at test doses decreased reactive oxygen species formation, preserved glutathione content and retained glutathione peroxide and catalase activities in high-glucose-treated HUVE cells (P < 0.05). Treatments with these extracts at 2 and 4% lowered interleukin-6, tumor necrosis factor-alpha and prostaglandin E2 production and reduced cyclooxygenase-2 activity (P < 0.05). CONCLUSION: These findings suggest that this vegetable could be considered as a functional food and might provide antioxidative and anti-inflammatory protection.

Protocatechuic acid inhibits lung cancer cells by modulating FAK, MAPK, and NF-κB pathways.

Cytotoxic effects of protocatechuic acid (PCA) upon 3 nonsmall cell lung cancer (NSCLC) cell lines, A549, H3255, and Calu-6 cell lines, were examined. PCA at 1, 2, 4, and 8 µM was used to treat these cells. Results showed that PCA dose-dependently reduced cell growth; and at 2-8 µM enhanced protein expression of Bax and cleaved caspase-3; as well as diminished Bcl-2 expression. This compound destabilized mitochondrial membrane via increasing caspase-3 activity, decreasing mitochondrial membrane potential and Na(+)-K(+)-ATPase activity in these cells. PCA treatments dose-dependently decreased protein expression of vascular endothelial growth factor and fibronectin, as well as lowered interleukin (IL)-6 and IL-8 release; and at 2-8 µM suppressed protein expression of basic fibroblast growth factor, matrix metalloproteinase (MMP)-2 and MMP-9. Furthermore, PCA treatments dose-dependently downregulated nuclear factor kappa (NF-κ)B p50 and NF-κB p65 protein expression, and at 2-8 µM suppressed protein expression of p-p38, p-JNK, and p-focal adhesion kinase (FAK). Our data revealed that PCA declined FAK, mitogen-activated protein kinase, and NF-κB activation, which subsequently decreased the production of cytokines and growth factors, and consequently inhibited proliferation of 3 test NSCLC cells. These findings suggest that PCA could provide wide-ranging anti-NSCLC potency.

Maslinic acid induces mitochondrial apoptosis and suppresses HIF-1α expression in A549 lung cancer cells under normoxic and hypoxic conditions.

The apoptotic effects of maslinic acid (MA) at 4, 8, 16, 32 and 64 µmol/L on human lung cancer A549 cells under normoxic and hypoxic conditions were examined. MA at 4-64 and 16-64 µmol/L lowered Bcl-2 expression under normoxic and hypoxic conditions, respectively (p < 0.05). This agent at 4-64 µmol/L decreased Na+-K+-ATPase activity and increased caspase-3 expression under normoxic conditions, but at 8-64 µmol/L it caused these changes under hypoxic conditions (p < 0.05). MA up-regulated caspase-8, cytochrome c and apoptosis-inducing factor expression under normoxic and hypoxic conditions at 8-64 µmol/L and 32-64 µmol/L, respectively (p < 0.05). MA down-regulated hypoxia-inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF), survivin and inducible nitric oxide synthase (iNOS) expression under normoxic and hypoxic conditions at 8-64 and 16-64 µmol/L, respectively (p < 0.05). After cells were pre-treated with YC-1, an inhibitor of HIF-1α, MA failed to affect the protein expression of HIF-1α, VEGF, survivin and iNOS (p > 0.05). MA at 8-64 and 32-64 µmol/L reduced reactive oxygen species and nitric oxide levels under both conditions (p < 0.05). These findings suggest that maslinic acid, a pentacyclic triterpenic acid, exerted its cytotoxic activities toward A549 cells by mediating mitochondrial apoptosis and the HIF-1α pathway.

Preventive effects of coixol, an active compound of adlay seed, in NGF-differentiated PC12 cells against beta-amyloid25-35-induced neurotoxicity.

Background: The health benefits of coixol, an active compound of adlay seed, have attracted certain attention. Adlay seed is often adopted in traditional Chinese medicine for the treatment of various inflammatory disorders. Thus, it is hypothesized that coixol could protect neuronal cells. Objectives: The preventive effects of coixol against Abeta25-35-induced damage in nerve growth factor-differentiated PC12 cells were explored. Methods: Differentiated PC12 cells were treated with coixol at 0.125 µM, 0.25 µM, 0.5 µM, 1 µM, and 2 µM for 48 h. Then, cells were further exposed to Abeta25-35 at 20 µM for 24 h. Results: Coixol treatments at 0.25-2 µM exhibited antiapoptotic effect via increasing Bcl-2 mRNA expression, mitochondrial membrane potential, and Na+-K+ ATPase activity as well as decreasing Bax mRNA expression, caspase-3 activity, and intracellular Ca2+ release. In addition, coixol treatments at 0.25-2 µM alleviated oxidative and inflammatory responses via lowering reactive oxygen species level, increasing glutathione content, promoting the activity of glutathione peroxidase, glutathione reductase, and catalase, decreasing the generation of tumor necrosis factor-α, interleukin (IL)-1ß, IL-6, and prostaglandin E2. Furthermore, coixol treatments at 0.25-2 µM diminished intracellular Ca2+ release, and restricted nuclear factor kappa B-binding activity and phosphorylation of p65 and p38. Coixol treatments at 0.5-2 µM increased protein generation of nuclear factor E2-related factor 2, and limited protein production of inducible nitric oxide synthase and receptor of advanced glycation end product. Conclusion: Our novel findings suggested that coixol was a compelling agent against beta-amyloid peptide-induced neurotoxicity.

Steamed daylily flower (Hemerocallis fulva L.) protected cardiac and hepatic cells against ethanol induced apoptotic and oxidative damage.

Our previous study examined the phytochemical composition and bio-activities of raw daylily flower (Hemerocallis fulva L.). However, this plant food is usually served via heat process such as cooking in a soup. This study aimed to investigate the phytochemical profile and biofunctions of steamed daylily flower (SDF). The content of total phenolic acids, total flavonoids, total carotenoids, total anthocyanins and total triterpenoids in SDF aqueous extract was assessed. Normal cardiac and hepatic cells, H9c2 and L-02 cells, were used to evaluate the protective effects of SDF against ethanol. SDF concentrations of 0.25%, 0.5%, and 1% were applied to treat H9c2 or L-02 cells for 48 h at 37 °C initially, followed by exposure to ethanol at 150 mM for 24 h at 37 °C. Results showed that the content of assessed phytochemicals was in the range of 1019-2045 mg/100 g dry weight. Flavonoids and triterpenoids were two major detected phytochemicals in SDF. SDF treatments at 0.5% and 1% increased the viability of H9c2 cells, but at three concentrations enhanced the survival of L-02 cells. SDF at 0.5% and 1% up-regulated Bcl-2 messenger RNA (mRNA) expression and down-regulated Bax mRNA expression. Ethanol increased reactive oxygen species production, decreased glutathione content, as well as lowered glutathione peroxidase and catalase activities. SDF treatments reversed these changes. SDF at 0.5% and 1% reduced the activity of cytochrome P450 2E1 and nicotinamide adenine dinucleotide phosphate oxidase, limited p47phox mRNA expression, as well as enhanced factor E2-related factor 2 and heme oxygenase-1 mRNA expression. SDF at three concentrations decreased gp91phox mRNA expression. In conclusion, these novel findings indicated that SDF aqueous extract was rich in phytochemicals and provided anti-apoptotic and anti-oxidative actions to protect cardiac and hepatic cells against ethanol. Thus, SDF might be considered as a functional food with multiple bio-activities.

Flavonoids protect pancreatic beta-cells from cytokines mediated apoptosis through the activation of PI3-kinase pathway.

The preventive effects of four phenolic compounds against cytokines-induced ß-cell destruction were assessed in this study. Treatment of INS-1 (832/13) cells with pro-inflammatory cytokine mixtures (interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ)) resulted in an increased apoptosis. While resveratrol or myricetin failed to prevent cell apoptosis, quercetin or naringenin treatment exhibited an about 40% less in cell death induced by cytokines-mediated damage. This protective effect of quercetin or naringenin might be mediated partially via the activation of the downstream pAkt and pBad pathways, an outcome which was abolished by pretreatment with a specific PI3-kinase inhibitor. Cellular protein levels of p-p38 MAPK and inducible NO synthase (iNOS) were enhanced after cytokines addition; however, the presence of quercetin or naringenin could not suppress their expression. While cytokines induced MnSOD, quercetin or naringnin did not further enhance expression of this protective protein. In addition, the loss of mitochondria membrane potential (MMP) after cytokines treatment might be partially corrected with quercetin or naringenin. However, none of the phenolic compounds tested in this study reversed the blunted glucose-stimulated insulin secretion after cytokines treatment. These results suggest that quercetin or naringenin might possibly be able to protect ß-cells from cytokines toxicity by enhancing cell survival through PI3-kinase pathway, independent of p-p38 MAPK or iNOS.

Trans fatty acids enhanced ß-amyloid induced oxidative stress in nerve growth factor differentiated PC12 cells.

The effects of trans fatty acids, elaidic acid (trans-9, C18:1) and linoelaidic acid (trans-9, trans-12 C18:2), at 20 or 40 µM in nerve growth factor differentiated PC12 cells with or without beta-amyloid peptide (Aß) were examined. Elaidic acid treatment alone did not affect cell viability and oxidative injury associated markers (P > 0.05). However, co-treatments of elaidic acid and Aß led to more reduction in mitochondrial membrane potential (MMP) and Na⁺-K⁺-ATPase activity, and more increase in DNA fragmentation and 8-hydroxydeoxyguanosine (8-OHdG) production than Aß treatment alone (P < 0.05). Linoelaidic acid alone exhibited apoptotic and oxidative effects in cells via decreasing MMP and Na⁺-K⁺-ATPase activity, increasing reactive oxygen species (ROS) level, lowering glutathione content and glutathione peroxidase (GPX) activity (P < 0.05). The co-treatments of linoelaidic acid with Aß further enhanced oxidative damage via enhancing the generation of ROS, nitrite oxide and 8-OHdG, elevating caspase-3, caspase-8 and nitric oxide synthase activities, as well as declining GPX, catalase and superoxide dismutase activities (P < 0.05). These results suggested that the interaction of linoelaidic acid and Aß promoted oxidative stress and impaired mitochondrial functions in neuronal cells.

Renal protective effects of extracts from guava fruit (Psidium guajava L.) in diabetic mice.

This study analyzed the content of phenolic acids and flavonoids in extracts of guava fruit (Psidium guajava L.), and examined the renal protective effects of guava aqueous extract (GAE) and ethanol extract (GEE) in diabetic mice. GAE had more caffeic acid, myricetin, and quercetin; and GEE had more cinnamic, coumaric and ferulic acids. GAE or GEE at 1 and 2 % was supplied in diet for 12 weeks. GAE or GEE intake at 2 % significantly reduced glucose and blood urea nitrogen levels, increased insulin level in plasma of diabetic mice (p < 0.05). GAE or GEE treatments dose-dependently reserved glutathione content, retained activity of catalase and glutathione peroxidase, and decreased reactive oxygen species, interleukin (IL)-6, tumor necrosis factor-α and IL-1ß levels in kidney (p < 0.05). GAE and GEE treatments at 2 % significantly declined renal N (ε)-(carboxymethyl)lysine, pentosidine and fructose levels (p < 0.05), and suppressed renal activity of aldose reductase (p < 0.05). These findings support that guava fruit could protect kidney against diabetic progression via its anti-oxidative, anti-inflammatory and anti-glycative effects.

WITHDRAWN: Anti-apoptotic and Anti-oxidative Effects of Aqueous Ex-tract Prepared from Steamed Daylily Flower on Normal Cardiac and Hepatic Cells against Ethanol

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Vitamins B status and antioxidative defense in patients with chronic hepatitis B or hepatitis C virus infection.

BACKGROUND & AIMS: The impact of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection upon B vitamins status and antioxidative defense in infected patients was examined. METHODS: Dietary record and blood levels of B vitamins and oxidative stress-associated biomarkers were determined for 195 healthy controls, 132 HBV, and 114 HCV patients. RESULTS: HBV-infected patients had significantly higher levels of total cholesterol, free fatty acids (FFA), and lower ghrelin level (p < 0.05); and HCV-infected patients had significantly higher Ishak inflammation score and lactate dehydrogenase activity (p < 0.05). HBV patients had significantly lower red blood cell (RBC) vitamins B(2) and B(6) levels, and HCV infection significantly decreased vitamins B(2,) B(6) and folate levels in RBC and/or plasma (p < 0.05). Correlation coefficients of RBC vitamin B(2) versus serum FFA in HBV patients, RBC vitamins B(2) and B(6) versus HCV RNA and Ishak inflammation score, and plasma vitamin B(6) vs Ishak inflammation score in HCV patients were <-0.5. HBV-infected patients had significantly higher oxidized glutathione level and lower glutathione peroxidase activity (p < 0.05), but HCV patients had significantly lower superoxide dismutase and catalase activities (p < 0.05). CONCLUSION: HBV or HCV infection enhanced oxidative stress and lowered B vitamins in circulation. In order to avoid other healthy risk, nutrition status should be monitored and limitation or supplementation of certain nutrients might be helpful for HBV- or HCV-infected patients.

Protective effects of an aqueous extract from pepino (Solanum muricatum Ait.) in diabetic mice.

BACKGROUND: This study analysed the content of ascorbic acid, phenolic acids and flavonoids in aqueous and ethanol extracts of pepino (Solanum muricatum Ait.), and examined the protective effects of pepino aqueous extract (PAE) in a mouse model of diabetes. PAE at 1, 2 and 4% was supplied for 5 weeks. RESULTS: Aqueous and ethanol extracts had similar levels of total phenolic acids, but PAE had a higher content of ascorbic acid and total flavonoids than the ethanol extract. PAE treatments at 2% and 4% significantly lowered plasma glucose level (P < 0.05); however, only the 4% PAE significantly elevated plasma insulin level at week 5 (P < 0.05). PAE treatments significantly decreased the levels of malonyldialdehyde and reactive oxygen species in kidney (P < 0.05); however, only the 2% and 4% treatments significantly reduced oxidised glutathione formation, increased glutathione level, and retained renal glutathione peroxidase and catalase activities (P < 0.05). PAE treatments at 2% and 4% significantly lowered renal interleukin (IL)-6 and tumour necrosis factor-α levels (P < 0.05); however, only the 4% treatments significantly diminished renal IL-1ß and levels of monocyte chemoattractant protein-1 (P < 0.05). PAE treatments at 4% significantly decreased aldose reductase activity and sorbitol production in kidney (P < 0.05). CONCLUSION: These findings support the suggestion that pepino aqueous extract could attenuate the progression of diabetes via its antioxidative, anti-inflammatory and antiglycative effects.

Aqueous extract prepared from steamed red amaranth (Amaranthus gangeticus L.) leaves protected human lens cells against high glucose induced glycative and oxidative stress.

HLE-B3 cell line, a human lens epithelial cell line, was used to examine the anti-glycative and anti-oxidative protection of aqueous extract prepared from steamed red amaranth leaves against high glucose induced injury. Phytochemical profile of this aqueous extract was analyzed. HLE-B3 cells were pretreated by this aqueous extract at 0.25%, 0.5%, or 1%, and followed by high glucose treatment. Results showed that the content of phenolic acids, flavonoids, anthocyanins, carotenoids, and triterpenoids in this aqueous extract was in the range of 1,107-2,861 mg/100 g dry weight. High glucose decreased cells viability and suppressed Bcl-2 mRNA expression. This aqueous extract pretreatments raised 11-42% cell survival and upregulated 20-47% Bcl-2 mRNA expression. High glucose reduced Na+ -K+ ATPase activity and mitochondrial membrane potential (MMP). This aqueous extract raised 27-40% Na+ -K+ ATPase activity, and 18-51% MMP. High glucose stimulated the generation of total advanced glycative endproducts (AGEs), methylglyoxal, and reactive oxygen species (ROS). This aqueous extract pretreatments lowered total AGEs, methylglyoxal, and ROS levels in the range of 0.38-1.17 folds, 1.7-4.9 nmol/mg protein, and 0.35-1.06 relative fluorescence unit/mg protein. High glucose upregulated mRNA expression of aldose reductase, nuclear factor kappa B, and p38. This aqueous extract pretreatments decreased mRNA expression of these factors in the range of 75-159%, 57-151%, and 54-166%. High glucose downregulated mRNA expression of nuclear factor E2-related factor 2 (Nrf2). This aqueous extract pretreatments increased 12-38% Nrf2 mRNA expression. These results suggested that this aqueous extract might be a potent nutritional supplement to prevent diabetic retinopathy.