Protective Effect Of Rutin Research Articles

Aflatoxin B1-induced hepatorenal impairment in rats via oxidative/inflammatory damage is accompanied by altered purinergic and kynurenine pathways: protective effect of rutin

Aflatoxin B1-induced hepatorenal impairment in rats via oxidative/inflammatory damage is accompanied by altered purinergic and kynurenine pathways: protective effect of rutin

Rutin mitigates fluoride-induced nephrotoxicity by inhibiting ROS-mediated lysosomal membrane permeabilization and the GSDME-HMGB1 axis involved in pyroptosis and inflammation

Fluoride is known to induce nephrotoxicity; however, the underlying mechanisms remain incompletely understood. Therefore, this study aims to explore the roles and mechanisms of lysosomal membrane permeabilization (LMP) and the GSDME/HMGB1 axis in fluoride-induced nephrotoxicity and the protective effects of rutin. Rutin, a naturally occurring flavonoid compound known for its antioxidative and anti-inflammatory properties, is primarily mediated by inhibiting oxidative stress and reducing proinflammatory markers. To that end, we established in vivo and in vitro models. In the in vivo study, rats were exposed to sodium fluoride (NaF) throughout pregnancy and up until 2 months after birth. In parallel, we employed in vitro models using HK-2 cells treated with NaF, n-acetyl-L-cysteine (NAC), or rutin. We assessed lysosomal permeability through immunofluorescence and analyzed relevant protein expression via western blotting. Our findings showed that NaF exposure increased ROS levels, resulting in enhanced LMP and increased cathepsin B (CTSB) and D (CTSD) expression. Furthermore, the exposure to NaF resulted in the upregulation of cleaved PARP1, cleaved caspase-3, GSDME-N, and HMGB1 expressions, indicating cell death and inflammation-induced renal damage. Rutin mitigates fluoride-induced nephrotoxicity by suppressing ROS-mediated LMP and the GSDME/HMGB1 axis, ultimately preventing fluoride-induced renal toxicity occurrence and development. In conclusion, our findings suggest that NaF induces renal damage through ROS-mediated activation of LMP and the GSDME/HMGB1 axis, leading to pyroptosis and inflammation. Rutin, a natural antioxidative and anti-inflammatory dietary supplement, offers a novel approach to prevent and treat fluoride-induced nephrotoxicity.

Rutin alleviated lipopolysaccharide-induced damage in goat rumen epithelial cells.

Rutin, also called vitamin P, is a flavonoids from plants. Previous studies have indicated that rutin can alleviate the injury of tissues and cells by inhibiting oxidative stress and ameliorating inflammation. There is no report on the protective effects of rutin on goat rumen epithelial cells (GRECs) at present. Hence, we investigated whether rutin can alleviate lipopolysaccharide (LPS)-induced damage in GRECs. GRECs were cultured in basal medium or basal medium containing 1 μg/mL LPS, or 1 μg/mL LPS and 20 μg/mL rutin. Six replicates were performed for each group. After 3-h culture, the GRECs were harvested to detect the relevant parameters. Rutin significantly enhanced the cell activity (p<0.05) and transepithelial electrical resistance (TEER) (p<0.01) and significantly reduced the apoptosis rate (p<0.05) of LPSinduced GRECs. Rutin significantly increased superoxide dismutase, glutathione peroxidase, and catalase activity (p<0.01) and significantly decreased lactate dehydrogenase activity and reactive oxygen species and malondialdehyde (MDA) levels in LPS-induced GRECs (p<0.01). The mRNA and protein levels of interleukin 6 (IL-6), IL-1β, and C-X-C motif chemokine ligand 8 (CXCL8) and the mRNA level of tumor necrosis factor-α (TNF-α) and chemokine C-C motif ligand 5 (CCL5) were significantly increased in LPS-induced GRECs (p<0.05 or p<0.01), while rutin supplementation significantly decreased the mRNA and protein levels of IL-6, TNF-α, and CXCL8 in LPS-induced GRECs (p<0.05 or p<0.01). The mRNA level of toll-like receptor 2 (TLR2), and the mRNA and protein levels of TLR4 and nuclear factor κB (NF-κB) was significantly improved in LPS-induced GRECs (p<0.05 or p<0.01), whereas rutin supplementation could significantly reduce the mRNA and protein levels of TLR4 (p<0.05 or p<0.01). In addition, rutin had a tendency of decreasing the protein levels of CXCL6, NF-κB, and inhibitor of nuclear factor kappa-B alpha (0.05< p<0.10). Rutin could significantly decreased interferon regulatory factor 3 mRNA expression in LPS-induced GRECs (p<0.05), whereas interferon induced protein with tetratricopeptide repeats 3 (IFIT3) and toll-interacting protein (TOLLIP) mRNA expression was not significantly different between the groups. LPS reduced the tight junction protein zonula occludin 1 (ZO-1) level in GRECs whereas rutin enhanced it. Rutin significantly improved tight junction protein Claudin-1 mRNA expression in LPS-induced GRECs (p<0.01), but could not affect tight junction protein Occludin mRNA expression. Rutin alleviated LPS-induced barrier damage in GRECs by improving oxidation resistance and anti-inflammatory activity, which may be related to TLR/NF-κB signaling pathway inhibition.

The antioxidant/anti-inflammatory protective effects of rutin against ethanol-induced testicular perturbation in rats: Involvement of the immunosuppressive indoleamine 2,3-dioxygenase.

This study investigated the influence of rutin against EtOH-induced testicular impairment in rats and the involvement of the indole-aminergic pathway. Four groups of eight rats each were orally exposed to drinking water (Group 1), EtOH (5 g/kg bwt, Group 2), R (5 g/kg bwt, Group 3), and EtOH + R (5 g/kg bwt + 50 mg/kg bwt, Group 4) via gavage for 15 days. Results showed that exposure to EtOH significantly (p < 0.0001) reduced the testicular antioxidant system and increased lipid peroxidation (LPO) relative to control. We observed a significant (p < 0.0001) increase in the inflammatory biomarkers, with attendant disruption in the testicular histological structure and concomitant elevation in the activities of indoleamine 2,3-dioxygenase (IDO), in comparison with control and no noticeable effects in tryptophan 2,3-dioxygenase (TDO) activity across the groups. Rutin-only exposed group did not show any alteration in the measured parameters when compared with the control. Rutin co-exposure augmented the antioxidant system, prevented histological damage, reduced LPO and inflammation, and thus, lowered EtOH-mediated increase in IDO activity, compared with control. Overall, these findings reveal the involvement of the indole-aminergic pathway in rutin's protective influence against EtOH-induced testicular impairment in rats.

Toxicity of copper and zinc alone and in combination in Caenorhabditis elegans model of Huntington's disease and protective effects of rutin

Copper (Cu) and Zinc (Zn) are required in small concentrations for metabolic functions, but are also toxic. There is a great concern about soil pollution by heavy metals, which may exposure the population to these toxicants, either by inhalation of dust or exposure to toxicants through ingestion of food derived from contaminated soils. In addition, the toxicity of metals in combination is questionable, as soil quality guidelines only assess them separately. It is well known that metal accumulation is often found in the pathologically affected regions of many neurodegenerative diseases, including Huntington's disease (HD). HD is caused by an autosomal dominantly inherited CAG trinucleotide repeat expansion in the huntingtin (HTT) gene. This results in the formation of a mutant huntingtin (mHTT) protein with an abnormally long polyglutamine (polyQ) repeat. The pathology of HD results in loss of neuronal cells, motor changes, and dementia. Rutin is a flavonoid found in various food sources, and previous studies indicate it has protective effects in HD models and acts as a metal chelator. However, further studies are needed to unravel its effects on metal dyshomeostasis and to discern the underlying mechanisms. In the present study, we investigated the toxic effects of long-term exposure to copper, zinc, and their mixture, and the relationship with the progression of neurotoxicity and neurodegeneration in a C. elegans-based HD model. Furthermore, we investigated the effects of rutin post metal exposure. Overall, we demonstrate that chronic exposure to the metals and their mixture altered body parameters, locomotion, and developmental delay, in addition to increasing polyQ protein aggregates in muscles and neurons causing neurodegeneration. We also propose that rutin has protective effects acting through mechanisms involving antioxidant and chelating properties. Altogether, our data provides new indications about the higher toxicity of metals in combination, the chelating potential of rutin in the C. elegans model of HD and possible strategies for future treatments of neurodegenerative diseases caused by the aggregation of proteins related to metals.

Protective Effect of Rutin and Vitamin E on Cobalt Chloride Induced Neurotoxicity

Toxic exposures to cobalt chloride could occur from dietary, occupational, and medical sources. This study evaluated the ameliorative effect of oral administration of rutin and vitamin E on cobalt chloride (CoCl2)-induced oxidative stress in the brain of rats following exposure to cobalt chloride (CoCl2) toxicity. Wistar rats were randomly divided into five groups. Group 1 received only water, while group 2 received cobalt chloride (300 ppm) in drinking water. Groups 3, 4 and 5 also received cobalt chloride, but were treated with rutin (100 mg/kg body weight), rutin (200 mg/kg BW) and vitamin E (50 mg/kg BW) respectively for seven consecutive days. The rats were euthanized 24 hours after the last treatment. The brain was collected for biochemical and histopathological evaluations. The study demonstrated that cobalt chloride caused a significant (P&lt;0.05) decrease in the activities of superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx) and glutathione level, whereas the levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) increased significantly (P&lt;0.05). However, rutin and vitamin E treatment attenuated CoCl2-induced oxidative stress. Histopathological findings also revealed the ameliorative effect of rutin and Vitamin E on the neuronal damage caused by CoCl2 treatment.

Protective effect of rutin on ferroptosis-induced oxidative stress in aging laying hens through Nrf2/HO-1 signaling.

Oxidative stress is a major cause of ovarian aging and follicular atresia. There is growing evidence that showed potential roles of rutin in antidiabetic, anti-inflammatory, antitumor, antibacterial and antioxidant, although it is yet unclear what the underlying mechanism is. Here, we looked into the potential effects of rutin on oxidative stress in the prehierarchical small white follicles (SWFs) from 580-day-old (D580) laying chickens. According to the findings, aging D580 layer ferroptosis was much higher than it was for laying hens during the peak period (280-day-old, D280). In both naturally aged and d-gal-induced chicken SWFs, rutin treatment concurrently boosted cell proliferation and prevented apoptosis. In addition, rutin inhibited the increased ferroptosis in aging hens. Meanwhile, rutin markedly suppressed the elevated ferroptosis and descending antioxidant capacity of D280-culture-SWFs from chicken elicited by d-gal. Rutin's activation of the Nrf2/HO-1 pathway hastened the SWFs' verbal battle with oxidative damage and reduced ferroptosis. Furthermore, activation of the ferroptosis signal increased the oxidative damage in SWFs. In conclusion, rutin alleviated oxidative stress that was induced by ferroptosis in aging chicken SWFs through Nrf2/HO-1 pathway. These findings point to a novel mechanism by which rutin protects SWFs from oxidative stress by suppressing ferroptosis, which is presumably a fresh approach to slowing ovarian aging in laying hens.

Protective Effect of Rutin on Triethylene Glycol Dimethacrylate-Induced Toxicity through the Inhibition of Caspase Activation and Reactive Oxygen Species Generation in Macrophages.

Rutin, also called quercetin-3-rhamnosyl glucoside, is a natural flavonol glycoside present in many plants. Rutin is used to treat various diseases, such as inflammation, diabetes, and cancer. For polymeric biomaterials, triethylene glycol dimethacrylate (TEGDMA) is the most commonly used monomer and serves as a restorative resin, a dentin bonding agent and sealant, and a bone cement component. Overall, TEGDMA induces various toxic effects in macrophages, including cytotoxicity, apoptosis, and genotoxicity. The aim of this study was to investigate the protective mechanism of rutin in alleviating TEGDMA-induced toxicity in RAW264.7 macrophages. After treatment with rutin, we assessed the cell viability and apoptosis of TEGDMA-induced RAW264.7 macrophages using an methylthiazol tetrazolium (MTT) assay and Annexin V-FITC/propidium iodide assay, respectively. Subsequently, we assessed the level of genotoxicity using comet and micronucleus assays, assessed the cysteinyla aspartate specific proteinases (caspases) and antioxidant enzyme (AOE) activity using commercial kits, and evaluated the generation of reactive oxygen species (ROS) using a dichlorodihydrofluorescein diacetate (DCFH-DA) assay. We evaluated the expression of heme oxygenase (HO)-1, the expression of nuclear factor erythroid 2 related factor (Nrf-2), and phosphorylation of AMP activated protein kinase (AMPK) using the Western blot assay. The results indicated that rutin substantially reduced the level of cytotoxicity, apoptosis, and genotoxicity of TEGDMA-induced RAW264.7 macrophages. Rutin also blocked the activity of caspase-3, caspase-8, and caspase-9 in TEGDMA-stimulated RAW264.7 macrophages. In addition, it decreased TEGDMA-induced ROS generation and AOE deactivation in macrophages. Finally, we found that TEGDMA-inhibited slightly the HO-1 expression, Nrf-2 expression, and AMPK phosphorylation would be revered by rutin. In addition, the HO-1 expression, Nrf-2 expression, and AMPK phosphorylation was enhanced by rutin. These findings indicate that rutin suppresses TEGDMA-induced caspase-mediated toxic effects through ROS generation and antioxidative system deactivation through the Nrf-2/AMPK pathway. Therefore, rutin has the potential to serve as a novel antitoxicity agent for TEGDMA in RAW264.7 macrophages.

Inhibitory potential of rutin on lipopolysaccharide-induced toxicity and inflammatory response of raw U937 cells and macrophages

Rutin is an important flavonoid found in plants with enormous pharmacological activities in various experimental models while lipopolysaccharide is an amphipathic glycolipid with potent inflammatory activity. The protective effect of rutin on lipopolysaccharide-mediated cytotoxity and inflammatory effect on U937 cells and macrophages was investigated. U937 cells were incubated with or without rutin (50 - 200 µM) and later exposed to lipopolysaccharide (5 µg/mL). Cell viability and the production of reactive oxygen species were later analyzed. In the other experiment, the cells were differentially-induced to macrophages and incubated with or without rutin before lipopolysaccharide exposure. The secretion of cytokines and expression of some transcription factors and enzymes were analyzed. It revealed that incubating cells with lipopolysaccharide alone caused significant cell death and production of reactive oxygen species which were reduced when cells were pre-incubated with rutin. Exposure of macrophages to lipopolysaccharide also resulted in significant secretion of both TNF-α and IL-6 which was reduced by rutin. Endotoxin also enhanced the expression of the transcription factors (NF-κB and iNOS) while reduced the expression of the antioxidant enzymes superoxide dismutase and catalase. The lipopolysaccharide-induced alterations in transcription were significantly reduced when macrophages were pre-incubated with rutin. Implications of the findings are discussed.

The protective effects of rutin on the liver, kidneys, and heart by counteracting organ toxicity caused by synthetic and natural compounds.

Rutin is a flavonoid present in many plant species. Because of its antioxidant, anti-inflammatory, and antiapoptotic properties, rutin is of interest for its potential protective effects against toxic agents. The hepatoprotective, renoprotective, and cardioprotective effects of rutin are reviewed. The antioxidant effects of rutin are elicited by enhancing antioxidant enzymes such as GST, GGT, CAT, GPx, SOD, and GR, activating the Nrf2/HO-1 pathway, elevating GSH content, and the reduction in MDA. The anti-inflammatory effects of rutin are mediated by the inhibition of IL-1β, IL-6, TGF-β1, COX-2, iNOS, TLR4, and XO. Rutin exerted its antiapoptotic effects by inhibition of free radicals, caspase-3/-7/-9, hsp70, HMGB1, and p53, and the elevation of the antiapoptotic protein Bcl-2. Rutin has potential therapeutic effectiveness against several toxicants, and its beneficial effects are more than likely mediated by its antioxidant, anti-inflammatory, and/or antiapoptotic property.

Rutin Suppresses DMBA Carcinogenesis in the Breast Through Modulating IL-6/NF-κB, SRC1/HSP90 and ER-α

Rutin dietary supplements may offer pharmacological benefits as anticancer and antiinflammatory properties. This study aimed to investigate the inhibitory and protective effect of rutin on signaling pathways of mammary gland carcinogenesis expermintally induced in female rats by 7,12-di-methyl benz (a) anthracene (DMBA). Results showed that rutin administration ameliorated DMBA toxicity and carcinogic effect on kidney and liver revealed by a significant decrease of urea and creatinine levels, and the activity of the liver enzymes alanine aminotransferase (ALT) and alkaline phosphatase (ALP). The antioxidant state indicated by the total antioxidant capacity (TAC) was significantly increased accompanied by a reduction in the inflammatory markers of interleukin-1β (IL-1B), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α) with induction of apoptosis indicated by a significant increase in caspase-3 level. Rutin significantly reduced the levels of the tumor markers carcinoma antigen 15-3 (CA 15-3) and proto-oncogene tyrosine-protein kinase Src1 (Src1). along with downregulation of nuclear factor-kB (NF-κB), heat shock protein 90 (HSP 90), and inducible nitric oxide synthase (iNOS) gene expression. The present study demonstrated the beneficial anticancer activity of rutin as a protective and therapeutic agent. Rutin induces its antitumor activity through elevation of the antioxidant state, inhibition of inflammatory cytokines, downregulation of oncogenes expression, and stimulation of apoptosis.

The effect of rutin on pulmonary contusion induced by blunt trauma in rats: Biochemical and histopathological evaluation.

Background This study aims to investigate the possible protective effects of rutin, also called vitamin P1, against pulmonary contusion induced by blunt chest trauma in a rat model. Methods Thirty male albino Wistar rats were separated into three equal groups as healthy group, trauma group, and trauma+rutin group. After anesthesia provided by intraperitoneal administration of 60 mg/kg ketamine and xylazine by inhalation at appropriate intervals, 200 g weight was dropped from 1 m height to the anterior chest wall of the animals in the trauma group (n=10) and trauma+rutin group (n=10) and pulmonary contusion was created. Thirty min after the trauma, 50 mg/kg of rutin was administered into the stomach of trauma+rutin group animals orally with gavage. The rats received rutin once daily for two days and were sacrificed 48 h later. Their lung tissues were removed and examined biochemically and histopathologically. Results Nuclear factor-kappa B, cyclooxygenase-2, and malondialdehyde levels increased in the trauma group compared to the healthy group, and rutin administration prevented this increase. Total glutathione levels decreased in the trauma group, and rutin administration also prevented this decrease. The histopathological findings were compatible with the biochemical findings. Conclusion Our study results suggest that rutin has a protective effect on contused lung tissue in rats.

Protective effect of rutin and β-cyclodextrin against hepatotoxicity and nephrotoxicity induced by lambda-cyhalothrin in Wistar rats: biochemical, pathological indices and molecular analysis

Background This study aimed to assess hepatotoxicity and nephrotoxicity of Lambda-cyhalothrin (LCT) and the protective effect of rutin alone and in combination with β-cyclodextrin (β–CD). Materials and methods Male Wistar rats were divided into five groups: Group 1: was used as a control and received a standard diet and water. Group 2, 3, 4 and 5 were orally administered with LCT (7.6 mg/kg body weight), rutin (200 mg/kg body weight) LCT and rutin (at the same doses as in Group 2 and Group 3), and LCT and a mixture of rutin with β-CD (400 mg/kg body weight), respectively. All experimental animals were orally gavaged 5 days/week for 60 days. Results Our data revealed that LCT-induced liver and kidney injuries were related to the up-regulated expression of TNF-α and down-regulated expression of NRF-2 genes mRNA, whereas these effects were reversed with rutin treatment. LCT-induced oxidative stress altered the histological picture, and the hematological and biochemical parameters. Conclusion Treatment with a rutin-β-CD complex had preventive potential against LCT via suppression of oxidative stress and augmentation of the antioxidant defense system.

Investigating Potential Protective Effects of Rutin against Deltametrin-Induced Spleen Toxicity in Rats through Oxidative Stress, Apoptosis and Inflammation Markers

Investigating Potential Protective Effects of Rutin against Deltametrin-Induced Spleen Toxicity in Rats through Oxidative Stress, Apoptosis and Inflammation Markers

The protective effect of rutin against the cisplatin-induced cochlear damage in vitro

Rutin is a natural flavonoid, with typical effects including interaction with enzymes and scavenging of free radicals. However, the role of rutin in the auditory system is still unclear. In the present study, we used neonatal organ of Corti explants in vitro to investigate the effects of rutin in cisplatin-induced ototoxicity. The TUNEL assay and the cleaved caspase-3 immunohistochemistry were used to detect the apoptosis of hair cell (HCs) in cochlear explants, and the MitoSox-Red staining was used to detect the difference in mitochondrial superoxide among different groups. Western blot was used to investigate the expression of genes. Confocal microscopy showed that after pretreatment with rutin, the accumulation of reactive oxygen species in HCs caused by cisplatin exposure was significantly reduced. Furthermore, the expression levels of p-P38 and p-JNK were significantly decreased, while ratio of p-AKT/AKT was significantly upregulated. Our study showed that rutin reduced cisplatin-induced HCs death in neonatal cochlear explants in vitro. The potential mechanism involved the alleviation of mitochondrial damage, the scavenging of reactive oxygen species (ROS), the suppression of MAPK signaling pathway, and the activation of PI3K/AKT signaling pathway.

The protective effect of rutin against lipopolysaccharide induced acute lung injury in mice based on the pharmacokinetic and pharmacodynamic combination model

Rutin is a flavonoid compound with many pharmacological activities, including antioxidation, anti-inflammation and cardiovascular and cerebrovascular protection. However, there are great limitations in clinical application in view of its poor solubility and slow absorption in vivo. In this study, a pharmacokinetic and pharmacodynomic model was adopted to study the correlation of the pharmacokinetics and pharmacodynomics of rutin in lipopolysaccharide-induced acute lung injury mice. Rutin was intragastrically administered continuously for 5 days at a dose of 200 mg/kg/d, and pharmacokinetic and pharmacodynamic indicators were measured every day after administration, including the blood concentration of rutin, the W/D ratio of lungs, the nitric oxide content and the expression levels of TLR4, TRAF6, IκB and P-IκB proteins. The results indicated that rutin can exert an anti-inflammatory protective effect by improving lung tissue injury, significantly decreasing the synthesis of the inflammatory mediator nitric oxide, and inhibiting the protein expression levels of TLR4, TRAF6 and P-IκB. The absorption of rutin conformed to a one-compartment model with the pharmacokinetic parameters as follows: t1/2α= 9.76 h, t1/2β= 19.44 h, Tmax= 24.00 h, Cmax= 22.65 μg/ml and AUC(0−t)= 518.58 μg/ml·h. A PK-PD combination model was established to fit the optimal administration time of rutin with a one-compartment-Sigmod Emax model connected to the effect site. Meanwhile,the PK-PD combination model was a better approach for evaluating the relationships between the five pharmacodynamic indicators and the pharmacokinetic characteristics of rutin. The correlation between the pharmacokinetics and pharmacodynamics of rutin was quantitatively analysed to provide a theoretical basis for the research and development of new anti-inflammatory drugs in clinical practice.

Antioxidant and anti-inflammatory protective effects of rutin and kolaviron against busulfan-induced testicular injuries in rats

ABSTRACT There are few treatment options, including the use of natural phenolics-based combination therapy for mitigating male infertility conditions associated with chemotherapy. Busulfan is an anti-cancer drug that leads to testicular problems in humans. Here, we studied the effect of co-treatment of rutin and kolaviron against busulfan-induced testis damage. Young adult male Wistar rats were intraperitoneally injected busulfan (4 mg/kg b.w), and then orally administered rutin (30 mg/kg b.w), and kolaviron (50 mg/kg b.w) alone and combined for 60 days. Results revealed that rutin and kolaviron alone or in combination reversed busulfan-induced increase in oxidative stress along with sperm quality of treated animals. However, kolaviron and rutin separately improved the concentrations of MDA and GSH and sperm quality more than when they were combined. Similarly, rutin and kolaviron separately or in combination preserved spermatogenesis and relieved busulfan-induced increase in nitric oxide concentration, myeloperoxidase and 3β-hydroxysteroid dehydrogenase activities. Co-supplementation with kolaviron but not rutin nor when rutin was combined with kolaviron also improved the testicular level of tumor necrosis-alpha. Finally, the histological features in the testes caused by busulfan were reversed by rutin, whereas treatment with kolaviron alone or in combination with rutin partially protected the testis from busulfan-induced injury as demonstrated by the appearance of few germ cells, damaged tubules, loss of round spermatids and defoliation of the seminiferous epithelium. Thus, the combined treatment regimen of rutin and kolaviron sparingly prevented busulfan-induced testicular injuries in rats. Abbreviations: CAT: Catalase; GSH: Glutathione; 3β-HSD: 3β- hydroxysteroid Dehydrogenase; MDA: Malondialdehyde; TNF-α: Tumor necrosis-alpha; BUS: Busulfan; RUT: Rutin; KV: Kolaviron; TBARS: Thiobarbituric Acid Reactive Substances; MPO: Myeloperoxidase; ELISA: Enzyme-Linked Immunoassay; NAD: Nicotinamide Adenine Dinucleotide (oxidized); ROS: Reactive Oxygen Species.

Anti Hemolytic Activity of Rutin incase of Phenyl Hydrazine induced Hemolysis

The important role of Red Blood Cells (RBCs) is to transport oxygen to the tissues from the lungs to provide oxygen to all cells. During circulation, RBCs are continuously exposed to both endogenous and exogenous sources of reactive oxygen species (ROS) that can injury the RBC and ruin its function. The imbalance between cellular production of reactive oxygen species and the counteracting antioxidant mechanism leads to Oxidative stress. Flavonoids are low molecular weight secondary polyphenolic metabolites present in plants characterized by their flavan nucleus. Rutin is a flavonol plentiful in a variety of commonly ingested foods. The term ‘Rutin’ came from a plant known as Ruta graveolens that also encompasses Rutin. Teas and fruits have high concentration of Rutin. Buckwheat seeds (Fagopyrum esculantum) are the richest source. Rutin protects the body from cellular damage caused by free radicals with its antioxidant properties. It helps to eliminate cholesterol from the body and increase elasticity of the arterial walls, which in turn promotes greater blood flow. The present investigation was aimed to assess the antihemolytic activity of the Rutin using phenyl hydrazine as hemolysin. This study uses RBC as model system to access the anti-hemolytic activity of Rutin using phenyl hydrazine as hemolysin. Phenyl hydrazine which was used previously in treating sickle cell anemia was used in this investigation as hemolysin. The result of the study shows that the addition of phenyl hydrazine [1-500 μg/ml] to the RBC suspension caused significant (P&lt;0.01) rise in hemolysis. The cell pellet in the bottom of the tubes reduced to reddish colored supernatant indicating hemolysis. The effect was concentration dependent. The present investigation clearly indicates that phenyl hydrazine causes hemolysis and toxicity to RBC. The concurrent addition of phenyl hydrazine along with the test compound Rutin (100-500 μg/ml) to the RBC suspension significantly (P&lt;0.01) reduced phenyl hydrazine induced hemolysis in a concentration dependent manner. The protective effect of Rutin on the hemolysis induced by phenyl hydrazine clearly shows it acts as anti-hemolytic agent. This finding was compared with the standard ascorbic acid. IC50 value of Rutin and ascorbic acid were 160.86 and 163.5 μg/ml respectively. The Rutin extract showed maximum inhibitory effect 69.8%.at 500μg/ml. This shows that Rutin can be effectively used as anti-hemolytic agent.

Oxidative and pro-inflammatory lung injury induced by desflurane inhalation in rats and the protective effect of rutin.

Desflurane is a mainstay of general inhaled anesthetics with a methyl ethyl ether structure and is widely used in clinical practice. It has been reported to induce inflammation and lipid peroxidation in rat pulmonary parenchyma, to increase alveolar macrophages, and to cause peribronchial infiltration and edema. Rutin, a flavonoid vitamin P1, is known to have biological properties including acting as an antioxidant, an anti-inflammatory, and an inhibitor of bronchoalveolar polymorphonuclear leukocyte (PNL) infiltration. The aim of this study is to examine the effects of rutin on desflurane-induced pulmonary injury using biochemical and histopathological methods. The rats were divided into 3 groups (n = 6 each): healthy control (HC), rutin+desflurane-treated (DRT) and desflurane-only (DSF). Briefly, 50 mg/kg of rutin was given orally to the DRT group and an equal volume of normal saline was given to the DSF and HC groups. After 1 h, anesthesia was induced and maintained in the DRT and DSF groups for 2 h. After the rats had been sacrificed, the lungs were removed. Malondialdehyde (MDA), total glutathione (GSH), tumor necrosis factor alpha (TNF-α), and nuclear factor kappa B (NF-κB) levels were measured in the excised lung tissue. The removed tissues were also fixed in 10% formalin, and the obtained sections were stained with hematoxylin and eosin (H&E) and evaluated under light microscopy. The biochemical and histopathological results of the DRT group were compared with those obtained from the DSF and HC groups. Desflurane increased MDA, TNF-α and NF-κB, and decreased GSH in lung tissue. The PNL infiltration, alveolar macrophages, hemorrhage, alveolar damage, and edema were observed in the lung tissue of the DSF group. Rutin was histopathologically shown to protect lung tissue from oxidative stress by preventing an increase in oxidant parameters and a decrease in antioxidants. The results suggest that rutin may be useful in the treatment of desflurane-associated lung injury.

The effect of Zinc Nanoparticles on Adult rat Prostate gland and the Possible Protective role of Rutin: histological and biochemical study

Abstract:Introduction: Zinc nanoparticles (ZnNPs) usage is evolving in different industrial and medical applications. However, recently nanoparticles were reported for their harmful effects. Rutin is a flavonoid that presents in plants, many veg‌etables, and fruits. It is considered a strong antioxidant.Aim: To detect the effect of ZnNPs on the adult rat prostate gland and evaluating the possible protective effect of Rutin. Materials & Methods: Fifty adult male albino rats were divided into four groups: Group I (control), Group II (ZnNPs group) rats received ZnNPs in a dose of 100 mg/kg via oral gavage feeding needle for 28 days. Group III (Rutin group): rats received rutin in a dose of 50 mg/kg via oral gavage feeding needle for 28 days. Group IV (ZnNPs- Rutin group): rats received Zn NPs and rutin at a dose and route as groups II, III. After 28 days, rats were weighed; blood samples were collected then sacrificed. The prostate glands were dissected and processed for histological (LM and EM), immunohistochemical, and biochemical studies with morphometric analysis. Results: Light microscopic examination of Group II sections revealed degeneration of acini, vacuolation, and pyknotic nuclei of their lining cells. A highly statistically significant increase in thickness of the fibromuscular stroma (P ˂ 0.001) in Masson Trichrome sections and a highly statistically significant increase (P ˂ 0.001) in positive PCNA immunoreactions in the nuclei of epithelial cells were detected. Ultrathin sections showed vacuolations in acinar cells cytoplasm. Those findings are associated with a highly significant increase in Malondialdehyde, and Prostatic specific antigen. On the contrary, Group IV sections displayed restoration of prostatic acini arrangement with areas of hyperplasia and a statistically decrease in MDA, PSA. Conclusion: These findings evidenced that Rutin had a natural protective role against ZnNPs induced prostatic cell injury in rats.