Evaluation of the Phytochemical and Pharmacological Potential of Taif's Rose (Rosa damascena Mill var. trigintipetala) for Possible Recycling of Pruning Wastes.

This study investigated the phytochemical contents of Taif's rose pruning wastes and their potential application as phytomedicine, thereby practicing a waste-recycling perspective. In the Al-Shafa highland, four Taif rose farms of various ages were chosen for gathering the pruning wastes (leaves and stems) for phytochemical and pharmacological studies. The leaves and stems included significant amounts of carbohydrates, cardiac glycosides, alkaloids, flavonoids, and other phenolic compounds. The cardiac glycoside and flavonoid contents were higher in Taif rose stems, while the phenolic and alkaloid contents were higher in the plant leaves. Cardiovascular glycosides (2.98-5.69 mg g-1), phenolics (3.14-12.41 mg GAE g-1), flavonoids (5.09-9.33 mg RUE g -1), and alkaloids (3.22-10.96 mg AE g-1) were among the phytoconstituents found in rose tissues. According to the HPLC analysis of the phenolic compounds, Taif's rose contains flavonoid components such as luteolin, apigenin, quercetin, rutin, kaempferol, and chrysoeriol; phenolics such as ellagic acid, catechol, resorcinol, gallic acid, and phloroglucinol; alkaloids such as berbamine, jatrorrhizine, palmatine, reticuline, isocorydine, and boldine. Warm water extract was highly effective against Bacillus subtilis, Escherichia coli, and Proteus vulgaris, whereas methanol and cold water extracts were moderately effective against Aspergillus fumigatus and Candida albicans. The study's findings suggested that Taif's rose wastes could be used for varied medical purposes.

Correlation between Apelin and Some Angiogenic Factors in the Pathogenesis of Preeclampsia: Apelin-13 as Novel Drug for Treating Preeclampsia and Its Physiological Effects on Placenta.

Preeclampsia (PE) is one of the commonest causes for maternal and fetal morbidity and mortality. Imbalances of angiogenic factors, oxidative stress, and inflammatory response have a role in the pathogenesis of PE. Data regarding the circulating apelin level and its role in PE remains controversial. This study was formulated to assess the serum apelin level in PE, investigate its correlation with some inflammatory, oxidative stress, and angiogenic proteins in a nitric oxide synthase inhibitor; the N (gamma)-nitro-L-arginine methyl ester (L-NAME)-induced rat model of PE and determine whether apelin administration could protect against development of PE. 40 healthy adult female albino rats and 10 adult male albino rats were used in this study. The pregnant female rats were randomly divided into three groups: group 1 (normal pregnant group), group 2 (PE-induced group), injected subcutaneously with 75 mg L-NAME/kg bodyweight/day starting from day 9 to 20 of gestation, and group 3 (PE-induced group supplemented with apelin (PE + apelin)); PE induced as before and simultaneously subcutaneously injected with apelin-13 (6 × 10-8 mol/kg bodyweight/twice daily) beginning from day 6 to 20 of gestation. In all groups, blood pressure and urine protein were determined at gestation days (GD) 0, 10, and 18. Moreover, serum apelin, placental growth factor (PLGF), vascular endothelial growth factor (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), interferon-gamma (IFN-γ), and interleukin-10 (IL-10) levels and serum superoxide dismutase enzyme (SOD) and catalase (CAT) activities of all groups were estimated at the end of experiment. Placental histopathological examination was also performed. PE-induced rats showed significantly decreased serum apelin levels. Moreover, they showed significantly increased blood pressures, urine proteins, sFlt-1, sEng, and IFN-γ (mean arterial blood pressure, urine proteins, sFlt-1, sEng, and IFN-γ showed significant negative correlations with serum apelin level), but it showed significantly decreased VEGF, PLGF, IL-10, SOD, and CAT (VEGF, PLGF, IL-10, and SOD showed significant positive correlations with serum apelin level). In contrast, exogenous apelin administration significantly ameliorated these parameters together with improvement in the placental histoarchitecture in the apelin-supplemented PE group. This study demonstrated the protective effects of apelin administration on the pathogenesis of PE.

In Situ Neutral System Synthesis, Spectroscopic, and Biological Interpretations of Magnesium(II), Calcium(II), Chromium(III), Zinc(II), Copper(II) and Selenium(IV) Sitagliptin Complexes.

Magnesium(II), calcium(II), chromium(III), zinc(II), copper(II), and selenium(IV) sitagliptin (STG) complexes-with the general formulas [Mg(STG)2(Cl)2]·6H2O, [Ca(STG)2(Cl)2], [Cr(STG)2(Cl)2]Cl.6H2O, [Zn(STG)2(Cl)2], [Cu(STG)2(Cl)2]·2H2O, and [Se(STG)2(Cl)2]Cl2, respectively-were designed and synthesized by the chemical reactions between metal(II, III, and IV) chloride salts with an STG ligand in situ methanol solvent in a 1:2 stoichiometric ratio (metal:ligand). Tentative structures of the complexes were proposed based on elemental analysis, molar conductance, magnetic moments, thermogravimetric analysis, and spectral (infrared, electronic, and 1H NMR) data. The particle size and morphological investigation were checked on the bases of scanning electron microscopy, transmission electron microscopy, and X-ray powder diffraction analyses. All the Mg2+, Ca2+, Cr3+, Zn2+, Cu2+, and Se4+ complexes were found to be six-coordinated, wherein the STG ligands act as bidentate chelating agents. This study demonstrates that pancreatic tissues are affected by the induction of experimental diabetes mellitus and clarifies the potential of the synthesized STG complexes, which was found to more significantly improve insulin secretion and the pancreatic and glycometabolic complications of diabetic rats than STG alone.

Chitosan and Lecithin Ameliorate Osteoarthritis Symptoms Induced by Monoiodoacetate in a Rat Model.

The present work aimed to assess the chondroprotective influence of chitosan and lecithin in a monoiodoacetate (MIA)-induced experimental osteoarthritis (OA) model. Forty male rats weighing 180-200 g were randomly distributed among the following five experimental groups (eight per group): control, MIA-induced OA, MIA-induced OA + chitosan, MIA-induced OA + lecithin, and MIA-induced OA + chitosan + lecithin. The levels of TNF-α, IL6, RF, ROS, and CRP, as well as mitochondrial markers such as mitochondrial swelling, cytochrome C oxidase (complex IV), MMP, and serum oxidative/antioxidant status (MDA level) (MPO and XO activities) were elevated in MIA-induced OA. Also, SDH (complex II) activity in addition to the levels of ATP, glutathione (GSH), and thiol was markedly diminished in the MIA-induced OA group compared to in control rats. These findings show that mitochondrial function is associated with OA pathophysiology and suggest that chitosan and lecithin could be promising potential ameliorative agents in OA animal models. Lecithin was more effective than chitosan in ameliorating all of the abovementioned parameters.

Zinc oxide nanoparticles with green tea extract complex in the pancreas of rats against monosodium glutamate toxicity.

OBJECTIVES: Nanotechnology is an exciting field for investigators. Green zinc oxide nanoparticles (ZnO NPs) with Camellia sinensis extract complex are proved to be used in the treatment of the toxicity of monosodium glutamate (MSG) in the liver, kidney, and testis of rats. Therefore, the synthesized complex of green nanoparticles using green tea extract (GTE) was tested against the toxicity of MSG on the pancreas. METHODS: The glucose and insulin levels were estimated as well as some biochemical parameters for evaluating the antioxidant status of the pancreas tissue. The histopathological change of the pancreas also has been determined. RESULTS: It indicates the biomedical capability of ZnO NPs/GTE to act as potent antidiabetic through decreasing blood glucose and increasing serum insulin also, inhibition of lipid peroxidation and enhancement of the antioxidant parameters. CONCLUSIONS: The ZnO NPs/GTE enhanced the pancreatic cell and Langerhans islets as well lowered the sugar levels and stimulated insulin.

Selenium and L-Carnitine Ameliorate Reproductive Toxicity Induced by Cadmium in Male Mice.

Cadmium (Cd) has been reported to reduce male fertility, impair reproductive capacity, and play a major role in the pathogenesis of infertility. This study was conducted to investigate the possible protective role of Selenium (Se) and L-carnitine (LC) against the adverse effects induced by Cd on the male reproductive system in mice. Animals were randomly divided into seven groups (n = 10); control group and six treated groups, as follows: Cd (0.35 mg/kg), Se (0.87 mg/kg), LC (10 mg/kg), and a combination of either Se or LC and then a combination of both with Cd, and all animals were injected for a period of 30 days. Exposure of Cd showed a significant decrease in enzymatic antioxidant activities, deficiency in reproductive performance, decrease serum testosterone level, severe changes in the histopathological architecture, and higher degree of damages and appearance of unblemished DNA strands. Treatment with Se and LC has the highly synergistic and ameliorates the damaging effect of Cd on the testis through the elevation of the enzymatic antioxidant and diminish histopathological abnormalities and DNA damage.

Ameliorative Role of Green Tea and Zinc Oxide Nanoparticles Complex Against Monosodium Glutamate-Induced Testicular Toxicity in Male Rats.

BACKGROUND AND OBJECTIVE: This study was designed to estimate the long-term effects of zinc oxide nanoparticles/green tea (ZnONPs/GTE) complex against monosodium glutamate (MSG). The antioxidant/oxidative status, testosterone levels, DNA damage, and histopathological changes of testis were evaluated. METHODS: The rats were divided into eight groups that were treated as follows: saline, the lower dosage of MSG (6.0 mg/kg), the higher dosage of MSG (17.5 mg/Kg), GTE, ZnONPs, ZnONPs/GTE and the last two groups were treated with the lower dosage of MSG or the higher dosage of MSG with ZnONPs/GTE complex. The data showed minimal toxicity in testicular tissue after the administration of ZnONPs. RESULTS: The MSG treatment in the adult male rats reduced testosterone levels and disrupted testicular histology, which revealed dose-dependence of MSG. Also, ZnONPs induced testicular dysfunction through the interference of antioxidant/oxidant balance and suppression of testosterone levels as well as induction of cellular damage of testis. The combination of ZnONPs with GTE complex significantly protects against MSG or ZnONPs toxicity by decreasing the DNA damage, oxidative stress, and enhancement of antioxidant as well as histological structure of testis. CONCLUSION: We could recommend using ZnONPs/GTE complex to reduce the toxicity of ZnONPs and MSG on the testis at the cellular and oxidative stress levels.

Evaluation of the Effect of Nanoparticles Zinc Oxide/Camellia sinensis Complex on the Kidney of Rats Treated with Monosodium Glutamate: Antioxidant and Histological Approaches.

BACKGROUND: Zinc oxide nanoparticles (ZnO NPs) are robustly used biomedicine. Moreover, no study has been conducted to explore the consequence of green synthesis of ZnO NPs with Camellia sinensis (green tea extract, GTE) on kidneys of rats treated with monosodium glutamate (MSG). METHODS: Therefore, the objective of the research was designed to explore the possible defensive effect of GTE/ZnO NPs against MSG-induced renal stress investigated at redox and histopathological points. RESULTS: The levels of urea and creatinine increased as the effect of a high dose of MSG, in addition, the myeloperoxidase and xanthine oxidase activates were elevated significantly with the high dose of MSG. The levels of non-enzymatic antioxidants (uric acid, glutathione, and thiol) were decreased sharply in MSG-treated rats as compared to the normal group. CONCLUSION: The data displayed that GTE/ZnO NPs reduced the effects of MSG significantly by reduction of the level peroxidation and enhancement intracellular antioxidant. These biochemical findings were supported by histopathology evaluation, which showed minor morphological changes in the kidneys of rats.

The Interaction of Zinc Oxide/Green Tea Extract Complex Nanoparticles and its Effect on Monosodium Glutamate Toxicity in Liver of Rats.

BACKGROUND: Zinc oxide nanoparticles (ZnO NPs) are increasingly utilized in both industrial and medical applications. Therefore, the study was aimed to investigate the effect of green nanoparticle complex (green tea extract/zinc oxide nanoparticles complex, GTE/ZnO NPs) on oxidative stress induced by monosodium glutamate (MSG) on the liver of rats. METHODS: Wistar male rats (n=64) weighing between 200-250 g were divided randomly into eight groups: control group was given physiological saline (1 mg/kg), two groups were treated with two different doses of MSG (MSG-LD, MSG-HD; 6 and 17.5 mg/Kg, respectively), GTE was given 1 mg/mL, 5th group was treated with ZnO NPs and 6th group was treated with GTE/ZnO NPs complex while, 7th and 8th groups were treated with MSG-LD + GTE/ZnO NPs complex and MSG-HD + GTE/ZnO NPs complex, respectively. All substances were given orally for 30 consecutive days. At the end of the study, the liver was homogenized for measurement of the oxidative stress status and anti-inflammatory biomarkers as well as histological and transmission alternations. RESULTS: Results showed that the antioxidant enzymes activity and glutathione level were significantly decreased in MSG groups than control in a dose-dependent manner. Conversely, the malondialdehyde and inflammatory cytokines levels were significantly increased in MSG groups than the control group. The liver indicated no evidence of alteration in oxidative status, anti-inflammatory and morphological parameters in GTE, ZnO NPs and GTE/ZnO NPs complex groups. CONCLUSION: In conclusion, MSG at both doses caused oxidative stress and inflammation on liver after 28 days of exposure that supported histological analysis and transmission view of hepatic parenchyma. GTE/ZnO NPs act as partial hepato-protective against MSG.

Antioxidant, antiapoptotic, antigenotoxic, and hepatic ameliorative effects of L-carnitine and selenium on cadmium-induced hepatotoxicity and alterations in liver cell structure in male mice.

L-carnitine (LC) and selenium (Se) have significant protective and antioxidant effects on several tissues. Cadmium (Cd), widely used in some industries and emitted from fossil fuels, is a heavy metal having a number of side effects, including hepatotoxicity. This study aims to assess the ameliorative function of both LC and SeCl4 on cadmium chloride (CdCl2)-induced liver toxicity. In total, 70 male mice included in this study were allocated to seven groups: control, CdCl2, LC, SeCl4, CdCl2 plus SeCl4, CdCl2 plus LC, CdCl2 plus SeCl4 and LC groups. Hepatic aminotransferase (aspartate aminotransferase [AST] and alanine transaminase [ALT]) activity and tumor necrosis factor-alpha [TNF-α] levels, as well as the antioxidant biomarkers (superoxide dismutase [SOD], glutathione reductase [GRx], glutathione-S-transferase [GST] and catalase [CAT], were examined. Histological and transmission electron microscopic [TEM] variations in the liver were used as indicators of liver damage after the administration of CdCl2-alone or CdCl2 with LC, SeCl4, or both. Genotoxic effects of CdCl2 were also evaluated and the possible roles of SeCl4 and/or LC on the expression of the antioxidant enzymes were studied. Results showed that administration of LC and SeCl4 decreased CdCl2-induced increase in ALT and AST levels and reduced oxidative stress to normal levels. In addition, LC combined with SeCl4 had a highly synergistic effect and elevated significantly the enzymatic antioxidants and decreased lipid peroxidation levels compared with those in the CdCl2-treated group. It is clear from the data that both LC and SeCl4 inhibit liver injury and improve the redox state in mice.

Protective effect of α-lipoic acid against spleen toxicity of dimethylnitrosamine in male mice: Antioxidant and ultrastructure approaches.

The α-lipoic acid is a soft material and useful for the potential biomedical applications. The study was aimed to assess the potency of α-lipoic acid (ALA) against the toxicity of dimethylnitrosamine (DMN) on spleen of mice by assessing the antioxidants, histopathological and ultrastructure changes. The experiment was achieved on six groups of male mice as following; groups 1, 2, 3, and 4 were served as a control, ALA groups, low dose of DMN (DMN-LD; 2mgkg-1) and high dose of DMN (DMN-HD; 4mgkg-1). Group 5 was received DMN-LD plus ALA and group 6 was given DMN-HD plus ALA. The results indicated that DMN elevated lipid peroxidation, xanthine oxidase, nitric oxide, and decline the antioxidant enzymes as well as raise the C-reactive protein and tumor necrosis factor. A critical obstruction was harmonized with a reduced in lymphocyte number in the white pulp were observed. All the lymphatic nodules appeared smaller in DMN-HD group. In spleen tissues, marked changes of rough endoplasmic reticulum and appearance of three large lymphocytes were noticed. ALA/DMN treatments were improved all the oxidative damage and the ultrastructure changes. The data evince that ALA was eliminated the adverse effects of DMN on spleen of mice.

Ameliorative effect of vitamin E and selenium against oxidative stress induced by sodium azide in liver, kidney, testis and heart of male mice.

The study purported to define the effects of daily administration of vitamin E (Vit E) and selenium (Se) on antioxidant enzyme activity in mice treated with high doses of sodium azide (SA). Male mice were randomly split into nine groups. Groups 1, 2 and 3 were injected daily with saline, Vit E, and Se, respectively, while groups 4, 5 and 6 administrated with different doses of SA (low, medium and high, respectively). The mice in groups 7, 8 and 9 received 100mg/kg Vit E, 17.5mg/kg Se, and a combination of Vit E and Se, respectively before the SA-treatment. Hepatic, renal, testis and heart, antioxidant enzymes as well as levels of lipid peroxidation and total antioxidant capacity levels were determined. Vit E alone affected on the antioxidant parameters of the examined tissues. Se had a preventive effect on the decrease of antioxidant parameters caused by SA and improved the diminished activities of all of them. The study demonstrates that a high dose of SA may alter the effects of normal level antioxidant/oxidative status of male mice and that Se is effective in reducing the SA-damage. Se acts as a synergistic agent with the effect of Vit E in various damaged caused by SA.

Oxidative stress, histopathological and electron microscopic alterations induced by dimethylnitrosamine in renal male mice and the protective effect of α-lipoic acid.

BACKGROUND: Dimethylnitrosamine (DMN) is a waste product of several industrial processes. α-Lipoic acid (ALA) is a vitamin-like chemical also called as an antioxidant. Therefore, the study was designed to investigate the potential benefits of ALA in reducing the nephropathy of DMN in male mice. METHODS: Animals were divided into 6 groups (n=8) and received their treatment for 4 weeks as follows: groups 1-4 served as control, ALA-treatment (16.12 mg/kg), DMN low dose treatment and DMN high dose treatment, respectively. Groups 5 and 6 received ALA before DMN low dose and DMN high dose, respectively. Superoxide dismutase, catalase, glutathione peroxidase and xanthine oxidase, total antioxidant capacity, nitric oxide, lipid peroxidation as well as the levels of uric acid and creatinine were determined. The histological and ultrastructure changes of renal tissue were also evaluated. RESULTS: Treatment of the DMN mice with ALA showed a reduction in the levels of kidney nitric oxide, lipid peroxidation, as well as creatinine and uric acid levels as compared with the DMN group. The results show that ALA plays an important role in quenching the free radicals resulting from the metabolism of DMN, thereby inhibiting lipid peroxidation and protecting membrane lipids from oxidative damage and, in turn, preventing oxidative stress and apoptosis. Histopathological and ultrastructure analysis of renal tissue confirmed the oxidative stress results occurred in DMN renal mice. Concomitant administration of ALA with DMN significantly decreased all the histopathological changes induced by DMN. CONCLUSIONS: The present study elucidated the therapeutic effects of ALA administered in combination with DMN to minimize its renal toxicity.

Effect of vitamin E and selenium separately and in combination on biochemical, immunological and histological changes induced by sodium azide in male mice.

Sodium azide (SA) is used as an active ingredient to control a broad spectrum of soil borne pathogens including insects, weeds, nematodes, fungi, and bacteria. The purpose of this study was to evaluate the ameliorator property of vitamin E (Vit E) or/and selenium (Se) against SA-induced injury in male mice at the biochemical, immunological and histological levels. The mice were divided into nine groups (10/group). The first three groups were served as control, Vit E and Se while, the second three groups were treated with three different doses of SA. The last three groups were treated with high dose of SA with Vit E or Se or Vit E and Se and all animals were treated for a period of 30 days. Exposure to SA at the three doses to mice led to an alternation of liver and kidney functions, decrease the testosterone concentration, decreased IgG and IgM levels as well as the increasing the TNF-α. The effects of SA on the biochemical parameters of mice were dose-dependent. Administration of Se or/and Vit E to SA-treated mice attenuates the toxicity of this compound, objectified by biochemical and histological improvement of liver, kidney and testis. But, the alleviation is more pronounced with the both antioxidants. Thus, the synergistic effect of Se and Vit E is most powerful in reducing the toxicity induced by SA and improving the humoral immune response of mice.

Monosodium glutamate induced testicular toxicity and the possible ameliorative role of vitamin E or selenium in male rats.

Monosodium glutamate (MSG) has been recognized as flavor enhancer that adversely affects male reproductive systems. The present study was carried out to evaluate the potential protective role of vitamin E (vit E) or selenium against MSG induced oxidative stress and histopathological changes in testis tissues of rats. Mature male Wistar rats weighing 150-200 g BW were allocated to evenly twelve groups each group of ten animals, the first group was maintained as control group, the 2nd, 3rd and 4th groups were administered MSG in three different dose levels (low, medium and high) (6, 17.5 and 60 mg/kg BW), the 5th and 6th groups were given vit E in two doses (low and high) (150 and 200 mg/kg), the 7th and 8th groups were administered selenium in two doses (low and high) (0.25 and 1 mg/kg) daily via gavage for a period of 30 days. Meanwhile the 9th and 10th groups were given combinations of MSG (high dose) and vit E while, the 11th and 12th groups were given MSG (high dose) plus selenium in two recommended doses for each one. Monosodium glutamate caused an elevation in lipid peroxidation level parallel with significant decline in SOD, CAT as well as GPx activities in testis tissues. Administration of vit E or selenium to MSG-treated groups declined lipid peroxidation, increased SOD, CAT, GPx activities. Selenium or vit E significantly reduced MSG induced histopathological changes by the entire restoration of the histological structures and the testicular antioxidant status to great extent in treated rats. In conclusion, supplementation of selenium or vit E could ameliorate the MSG induced testicular toxicity to great extent and reduce the oxidative stress on testis tissues.