Role of Eruca sativa L. seeds in boosting the reproductive performance of male Japanese quails (Coturnix c. japonica).

Herein we attempt to shed light on the potential improving effect of Eruca sativa seeds (ESS) on the reproductive aspects of male Japanese quails. To accomplish this objective, two groups of quails were supplemented with ESS powder at doses of 5 and 10 g/kg feed from 7 days to 140 days of age, in addition to the control group, which did not receive treatment. Forty males were reared singly in cages to evaluate sperm characters and 32 males were raised with 64 females to evaluate fertility and sperm penetrability. Sixty-six phytochemical compounds were found according to gas chromatography-mass spectrometry analysis of ESS. The most plentiful ones are 13-docosenoic acid methyl ester, 9-octadecenoic acid methyl ester, and linoleic acid methyl ester. Both 5 g/kg and 10 g/kg doses of ESS showed similar effectiveness in enhancing various reproductive parameters, including gonadal index, sperm characteristics, fertility, libido, and cloacal gland attributes. However, some aspects like sperm concentration and testosterone levels exhibited a dose-dependent response. There is no significant change in mortality rate of supplemented groups compared to the control one. ESS also caused a reduction in feed intake and an enhancement in feed conversion ratio without affecting final body weight and body weight gain. This suggests potential nutritional benefits beyond reproductive health. The low-dose-fed group showed a significant reduction in total cholesterol and malondialdehyde compared to the high-dose-fed and unfed groups. The higher dose notably increased total antioxidant capacity compared to the lower dose and control group. Despite the positive effects on male reproductive parameters, there wasn't a significant impact on hatchability percentage, indicating that while male fertility improved, it might not have directly affected the viability of the eggs. Overall, the study suggests that ESS could be a safe and promising addition to the diet of male Japanese quails to enhance their reproductive capabilities without adverse effects. The findings could have implications for poultry farming by potentially improving breeding efficiency and health outcomes in quails.

Gallic acid rescues uranyl acetate induced-hepatic dysfunction in rats by its antioxidant and cytoprotective potentials.

BACKGROUND: The liver was identified as a primary target organ for the chemo-radiological effects of uranyl acetate (UA). Although the anti-oxidant and anti-apoptotic properties of gallic acid (GA) make it a promising phytochemical to resist its hazards, there is no available data in this area of research. METHODS: To address this issue, eighteen rats were randomly and equally divided into three groups. One group was received carboxymethyl cellulose (vehicle of GA) and kept as a control. The UA group was injected intraperitoneally with UA at a single dose of 5 mg/kg body weight. The third group (GA + UA group) was treated with GA orally at a dose of 100 mg/kg body weight for 14 days before UA exposure. UA was injected on the 15th day of the experiment in either the UA group or the GA + UA group. The biochemical, histological, and immunohistochemical findings in the GA + UA group were compared to both control and UA groups. RESULTS: The results showed that UA exposure led to a range of adverse effects. These included elevated plasma levels of aspartate aminotransferase, lactate dehydrogenase, total protein, globulin, glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and very-low-density lipoprotein and decreased plasma levels of high-density lipoprotein cholesterol. The exposure also disrupted the redox balance, evident through decreased plasma total antioxidant capacity and hepatic nitric oxide, superoxide dismutase, reduced glutathione, glutathione-S-transferase, glutathione reductase, and glutathione peroxidase and increased hepatic oxidized glutathione and malondialdehyde. Plasma levels of albumin and alanine aminotransferase did not significantly change in all groups. Histopathological analysis revealed damage to liver tissue, characterized by deteriorations in tissue structure, excessive collagen accumulation, and depletion of glycogen. Furthermore, UA exposure up-regulated the immuno-expression of cleaved caspase-3 and down-regulated the immuno-expression of nuclear factor-erythroid-2-related factor 2 in hepatic tissues, indicating an induction of apoptosis and oxidative stress response. However, the pre-treatment with GA proved to be effective in mitigating these negative effects induced by UA exposure, except for the disturbances in the lipid profile. CONCLUSIONS: The study suggests that GA has the potential to act as a protective agent against the adverse effects of UA exposure on the liver. Its ability to restore redox balance and inhibit apoptosis makes it a promising candidate for countering the harmful effects of chemo-radiological agents such as UA.

Gum Arabic nanoformulation rescues neuronal lesions in bromobenzene-challenged rats by its antioxidant, anti-apoptotic and cytoprotective potentials.

Bromobenzene (BB) is a hazardous environmental contaminant because of its multiple routes of exposure and the toxicity of its bio-derivates. It could elicit neuronal alterations by stimulating redox imbalance and apoptotic pathways. Gum Arabic (GA) protected the hippocampus of a type 2 diabetic rat model from cognitive decline. Whether gum Arabic nanoemulsion (GANE) can increase the neuroprotectant potency of GA in fighting BB-associated neurological lesions is the question to be answered. To accomplish this objective, 25 adult male Wistar rats were randomly and equally assigned into five groups. Control received olive oil (vehicle of BB). BB group received BB at a dose of 460 mg/kg BW. Blank nanoemulsion (BNE) group supplemented with BNE at 2 mL of 10% w/v aqueous suspension/kg BW. GANE group received GANE at a dose of 2 mL of 10% w/v aqueous suspension/kg BW. BB + GANE group exposed to BB in concomitant with GANE at the same previous doses. All interventions were carried out daily by oral gavage for ten consecutive days. BB caused a marked increase in malondialdehyde and succinate dehydrogenase together with a marked decrease in reduced glutathione, glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase, and lactate dehydrogenase in the brain. BB was accompanied by pathological deteriorations, amyloidosis, and reduced immuno-expression of integrase interactor 1 in the hippocampal region. Administration of GANE was beneficial in reversing the aforementioned abnormalities. These results pave the road for further discovery of nano-formulated natural products to counter the threats of BB.

Berberine protects against diclofenac sodium-induced testicular impairment in mice by its anti-oxidant and anti-apoptotic activities.

Objectives: This study was designed to investigate the effect of berberine (BBR) on diclofenac sodium-induced testicular impairment in mice. Materials and Methods: Eighteen male mice were divided randomly and equally into three groups for three weeks. One group was kept as control, the second group was injected intraperitoneally with diclofenac sodium (DS) at a dose of 10 mg/kg BW daily during the second and third weeks. The third group received daily oral administration of BBR at a dose of 50 mg/kg BW throughout the whole period of the experiment in parallel with the injection of the above-mentioned dose of DS during the second and third weeks. Plasma testosterone as well as testicular lipid peroxides (LPO), nitric oxide (NO), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were evaluated. In paraffin-embedded testicular tissues, histological examination, immuno-expression of glutathione reductase (GR), and TUNEL assay were carried out. Results: Testosterone levels were within the normal range in all groups. BBR decreased testicular LPO and induced SOD and GSH without marked changes in CAT and NO. The histology of testis was improved and, regularity and integrity of seminiferous tubules basement membranes, and distribution and amount of peritubular collagen fibers were normalized. BBR treated group showed few positive GR immuno-expression in spermatogenic cells and negative GR immuno-expression in interstitial cells of Leydig along with a few apoptotic spermatogenic cells. Conclusion: BBR is effective in protecting against DS-induced testicular dysfunction by improving oxidant/anti-oxidant balance and blocking the apoptotic cascade.

Induction of liver fibrosis by CCl4 mediates pathological alterations in the spleen and lymph nodes: The potential therapeutic role of propolis.

In an animal models, carbon tetrachloride (CCl4) is a carcinogenic agent that causes liver fibrosis. The current study aims to investigate whether induction in liver-fibrosis by CCl4 in the mouse model could promote the initiation of fibrosis in lymph node and spleen due to sustained increase of inflammatory signals and also aimed to clarify the protective therapeutic effects of propolis. The male mice (BALB/c) were categorized into three experimental sets and each group involved 15 mice. Control group falls into first group; group-II and group-III were injected with CCl4 to induce liver-fibrosis and oral supplementation with propolis was provided in group-III for 4-weeks. A major improvement with hepatic collagen and α-smooth muscle actin (α-SMA) production was aligned with the activation of liver fibrosis from CCl4. Mice treated with CCl4 exhibited collagen deposition towards liver sections, pathological alterations in spleen and lymph node architectures, and a significantly increase the circulation of both T&B cells in secondary lymphoid organs. Mechanically, the secondary lymphoid organs treated with CCl4 in mice exposed a positive growth in α-SMA and collagen expression, increased in proinflammatory cytokine levels and a significant increase in TGF-ß, NO and ROS levels. A manifest intensification in the expression of Nrf2, COX-2, and eNOS and upregulation of ASK1 and P38 phosphorylation. Interestingly, addition of propolis-treated CCl4 mice, substantially suppressed deposition of liver collagen, repealed inflammatory signals and resorted CCl4-mediated alterations in signaling cascades, thereby repairing the architectures of the secondary lymphoid organs. Our findings revealed benefits of propolis against fibrotic complications and enhancing secondary lymphoid organ architecture.

Effect of zinc oxide nanoparticles on broilers' performance and health status.

The current study investigated the effects of zinc oxide nanoparticles (ZONPs) and oxytetracycline (OTC) supplementation on broilers' behavior, performance, carcass quality, biochemical parameters, and intestinal microbial populations and birds' response to Newcastle disease (ND) vaccine. A total of 336 seven-day-old IR broiler chicks were randomly allotted to six dietary treatments containing 0, 10, 20, 30 and 40 ppm ZONPs or 50 ppm OTC. Each diet was fed to 7 replicates (8 birds/pen). The results clarified that 10 ppm ZONPs significantly improved the body weight gain and feed conversion in comparison to the control. No changes in behavior were recorded. The 10 ppm and 30 ppm ZONPs and OTC significantly reduced the gizzard weight in comparison to the control. While, 10 ppm ZONPs significantly increased the spleen weight, and all ZONPs doses increased bursa weight in comparison to the control and OTC groups. 20 ppm ZONPs increased the eviscerated yield and edible yield in comparison to the control and OTC groups. 40 ppm ZONPs increased pH, reduced meat color and overall acceptability in comparison to the control. In addition, results revealed that the 20 ppm ZONPs increased Calcium (Ca), High density low cholesterol (HDL-C), reduced urea (UA) and triglyceride (TG). Also, 40 ppm ZONPs and OTC increased creatinine (Cr) and reduced ND-HI titer in comparison to the control. For microbial population, OTC group was significantly lower than ZONPs groups in the total anaerobic, aerobic and lactobacilli count. In conclusion, the dietary inclusion of ZONPs can be applied as antibiotic growth promoter substitutions in broilers' diet. However, further investigations are still needed.

The Therapeutic Mechanisms of Propolis Against CCl4 -Mediated Liver Injury by Mediating Apoptosis of Activated Hepatic Stellate Cells and Improving the Hepatic Architecture through PI3K/AKT/mTOR, TGF-ß/Smad2, Bcl2/BAX/P53 and iNOS Signaling Pathways.

BACKGROUND/AIMS: Propolis is one of the most promising natural products, exhibiting not only therapeutic but also prophylactic actions. Propolis has several biological and pharmacological properties, including hepatoprotective activities. The present study aimed to investigate the underlying molecular mechanisms of propolis against CCl4-mediated liver fibrosis. METHODS: Three groups of male BALB/c mice (n=15/ group) were used: group 1 comprised control mice; groups 2 and 3 were injected with CCl4 for the induction of liver fibrosis. Group 3 was then orally supplemented with propolis (100 mg/kg body weight) for four weeks. Different techniques were used to monitor the antifibrotic effects of propolis, including histopathological investigations using H&E, Masson's trichrome and Sirius red staining; Western blotting; flow cytometry; and ELISA. RESULTS: We found that the induction of liver fibrosis by CCl4 was associated with a significant increase in hepatic collagen and α-smooth muscle actin (α-SMA) expression. Moreover, CCl4-treated mice also exhibited histopathological alterations in the liver architecture. Additionally, the liver of CCl4-treated mice exhibited a marked increase in proinflammatory signals, such as increased expression of HSP70 and increased levels of proinflammatory cytokines and ROS. Mechanistically, the liver of CCl4-treated mice exhibited a significant increase in the phosphorylation of AKT and mTOR; upregulation of the expression of BAX and cytochrome C; downregulation of the expression of Bcl2; a significant elevation in the levels of TGF-ß followed by increased phosphorylation of SMAD2; and a marked increase in the expression of P53 and iNOS. Interestingly, oral supplementation of CCl4-treated mice with propolis significantly abolished hepatic collagen deposition, abrogated inflammatory signals and oxidative stress, restored CCl4-mediated alterations in the signaling cascades, and hence repaired the hepatic architecture nearly to the normal architecture observed in the control mice. CONCLUSION: Our findings revealed the therapeutic potential and the underlying mechanisms of propolis against liver fibrosis.

Uranium exposure increases spermatocytes metaphase apoptosis in rats: inhibitory effect of thymoquinone and N-acetylcysteine.

Uranyl acetate (UA), a commercial stock from depleted uranium (DU), has a combined effect of chemical toxicity and mild radioactivity. Here, we investigated the potential antioxidant, antiapoptotic and cytoprotective effects of thymoquinone (TQ) and N-acetylcysteine (NAC) against UA-induced testicular damage in rats. UA reduced testicular superoxide dismutase (SOD) activity and nitric oxide (NO) and glutathione (GSH) levels relative to the control group. Interestingly, the testicular SOD activity and NO and GSH levels of UA/TQ- and UA/NAC-treated groups were also significantly lower relative to the control. A marked increase in spermatocytes metaphase apoptosis was found (stage XIII) in UA-treated rats, which is probably due to difficulties in segregation of homologous-chromosomes. This may clarify why UA exposure decreased round spermatids numbers and fertility in previous studies. To check the reason of partial metaphase arrest, the presence of DNA-damage-related γ-H2AX foci in late spermatocytes of all groups was checked, but only insignificant increase was found in UA-treated group. TQ or NAC supplementation reduced the apoptosis and improved the testicular histological alterations. Thus, TQ and NAC attenuate UA adverse effects on the testicular microenvironement through anti-apoptotic and cytoprotective but not antioxidant effects.

Maternal supplementation of diabetic mice with thymoquinone protects their offspring from abnormal obesity and diabetes by modulating their lipid profile and free radical production and restoring lymphocyte proliferation via PI3K/AKT signaling.

BACKGROUND: Epidemiological studies have shown that the offspring of mothers who experience diabetes mellitus during pregnancy are seven times more likely to develop health complications than the offspring of mothers who do not suffer from diabetes during pregnancy. The present study was designed to investigate whether supplementation of streptozotocin (STZ)-induced diabetic pregnant mice with thymoquinone (TQ) during pregnancy and lactation improves the risk of developing diabetic complications acquired by their offspring. METHODS: Three groups of pregnant female mice were used: non-diabetic control dams (CD), diabetic dams (DD), and diabetic dams supplemented with TQ (DD + TQ) during pregnancy and lactation (n = 10 female mice in each group). RESULTS: Our data demonstrated a marked decrease in the number of neonates born to DD, and these neonates showed a marked increase in their mean body weight (macrosomic pups) compared to those born to CD and DD + TQ. The induction of diabetes during pregnancy and lactation resulted in macrosomic pups with several postpartum complications, such as a marked increase in their levels of blood glucose, free radicals, plasma pro-inflammatory cytokines (IL-1ß, IL-6, and TNF-α), and lipids, and a tendency toward abnormal obesity compared to the offspring of CD. By contrast, macrosomic offspring born to DD exhibited a marked reduction in plasma cytokine levels (IL-2, -4 and -7), an obvious reduction in the number of circulating lymphocytes, decreased proliferation of superantigen (SEB)-stimulated lymphocytes and aberrant AKT phosphorylation. Interestingly, the supplementation of DD with TQ during pregnancy and lactation had an obvious and significant effect on the number and mean body weight of neonates. Furthermore, TQ significantly restored the levels of blood glucose, insulin, free radicals, plasma cytokines, and lipids as well as lymphocyte proliferation in the offspring. CONCLUSIONS: Our data suggest that the nutritional supplementation of DD with the natural antioxidant TQ during pregnancy and lactation protects their offspring from developing diabetic complications and preserves an efficient lymphocyte immune response later in life.

Type I interferon (IFN-alpha/beta) rescues B-lymphocytes from apoptosis via PI3Kdelta/Akt, Rho-A, NFkappaB and Bcl-2/Bcl(XL).

Although IFN-alpha was reported to promote the survival of peripheral B-lymphocytes via the PI3-kinase-Akt pathway, the triggered signalling pathways involved in the protection of B cell from apoptosis need to be clarified. Using flow cytometry and western blot analysis, we have found that type 1 IFNs (IFN-alpha/beta) protect human B cells in culture from spontaneous apoptosis and from apoptosis mediated by anti-CD95 agonist, in a dose- and time-dependant manner. IFN-alpha/beta-mediated anti-apoptotic effect on human B cells was totally abrogated by blockade of IFNR1 chain. Our data indicate that PI3Kdelta, Rho-A, NFkappaB and Bcl-2/Bcl(XL) are active downstream of IFN receptors and are the major effectors of IFN-alpha/beta-rescued B cells from apoptosis. Furthermore, immunohistochemical results show marked reduction in numbers of CD20 positive B cell in both spleen and Peyer's patches from mice treated with anti-IFNR1 blocking antibody compared with control group. Moreover, ultrastructural observations of these organs show an obvious increase in apoptotic cells from mice treated with anti-IFNR1 blocking antibody. Our results provide more details about the triggered signalling pathways and the phosphorylation cascade which are involved in the protection of B cell from apoptosis after treatment with IFN-alpha/beta.

Blocking type I interferon (IFN) signaling impairs antigen responsiveness of circulating lymphocytes and alters their homing to lymphoid organs: protective role of type I IFN.

BACKGROUND: We recently demonstrated that type I Interferon (IFN) rescues in vitro, human B-lymphocytes from apoptosis via PI3Kδ/Akt, Rho-A, NFκB and Bcl-2/BclXL. In the present study we extended our work to clarify, in vivo, the role of type I IFN signalling on the circulating and lymphoid organs homing lymphocytes. METHODOLOGY: Two groups of mice 13 in each were set: type I IFN signalling blocked mice injected with anti-IFNAR1 antagonist antibody (10 mg/kg body weight) once/day for up to 20 days, and control group were injected with vehicle alone. RESULTS: Flow cytometry analysis to monitor the blood lymphocyte phenotype and proliferation have shown a significant decrease in CD45R/B220(+) [corrected] B cells, CD4(+) and CD8(+) T cells in treated animals. Furthermore, the proliferative capacities of these lymphocyte subsets were significantly decreased in treated animals compared to those of control mice. Marked reduction in the plasma levels of IL-2 and IL-7 (cytokines important for the development of T and B cells) but not of IL-6 or IL-10 was observed in treated mice and this may a cause for emergence decrease in B and T cell numbers. Immunohistochemical studies have further shown a marked reduction in the numbers of CD20(+) B cells in spleen and Peyer's patches and CD3(+) T cells in thymus of treated animals. Moreover, electron microscopy examinations have revealed a loss of lymphocytes with characteristic features of apoptosis. CONCLUSION: Our data confirmed that the in vivo inhibition of type I IFN signaling induce decrease in the numbers and defective functions of circulating and lymphoid organs homing lymphocytes providing a strong evidence for the protective effects of type 1 IFNs (IFN-α/ß) on B and T lymphocytes.