Effects of ginger extract and/or propolis extract on immune system parameters of vaccinated broilers.

Newcastle disease (ND), avian influenza (AI, H5N8), and infectious bronchitis (IB) are important diseases in the poultry industry and cause significant losses. Vaccination is the most practical method for controlling infectious diseases. To reduce vaccination costs and several disorders in poultry farms, using herbal water supplements for immunomodulation with vaccination is critical to improving or preventing some conditions in the poultry industry. However, drinking water supplementation of ginger extract (GE)/propolis extract (PE) alone/in combination may increase broilers' humoral and cellular immunity due to the immunomodulatory effects of ginger and propolis. This protocol aimed to see how GE/PE alone or in combination improved the immunity, immune organ gene expression, and histology of the immune organs of broilers for 35 d after vaccination against NDV, H5N8, IBV, and IBDV. The chicks were dispensed into 5 groups according to GE and/or PE with vaccination. The control group was offered normal drinking water without any supplements or vaccinations. The GE group was supplemented with ginger extract (1 mL/L drinking water) in the drinking water before and after vaccination for 2 and 3 d, respectively. The GE+PE group was supplemented with GE (0.5 mL/L drinking water) and PE (0.5 mL/L drinking water) in the drinking water before and after vaccination for 2 and 3 d, respectively. The PE group was supplemented with propolis extract (1 mL/L drinking water) in the drinking water before and after vaccination for 2 and 3 d, respectively. The fifth group was the vaccinated untreated group. This experiment showed the immunomodulatory properties of GE and/or PE against 3 common diseases, NDV, AI, and IB, in broiler chicken farms for 35 d applied to a vaccination program. Thus, ginger extract and propolis extract supplementation in drinking water increased antibody titer, INF, IL10, and IL2 and TLR3 gene expression in the bursa of Fabricius, thymus, and spleen, respectively, as well as cellular immunity as indicated by increased CD3, CD4, and CD8 in the bursa of Fabricius, thymus, and spleen, respectively, with normal lymphocytes in the medulla of the bursa, thymus, and spleen. In conclusion, propolis extracts alone or with GE improved all of the metrics mentioned above without harming the histology of the immune organs.

Ameliorative effect of nanocurcumin and Saccharomyces cell wall alone and in combination against aflatoxicosis in broilers.

BACKGROUND: The adverse effect of aflatoxin in broilers is well known. However, dietary supplementation of Saccharomyces cell wall and/or Nanocurcumin may decrease the negative effect of aflatoxin B1 because of the bio-adsorbing feature of the functional ingredients in Yeast Cell Wall and the detoxification effect of curcumin nanoparticles. The goal of this study was to see how Saccharomyces cell wall/Nanocurcumin alone or in combination with the aflatoxin-contaminated diet ameliorated the toxic effects of aflatoxin B1 on broiler development, blood and serum parameters, carcass traits, histology, immune histochemistry, liver gene expression, and aflatoxin residue in the liver and muscle tissue of broilers for 35 days. Moreover, the withdrawal time of aflatoxin was measured after feeding the aflatoxicated group an aflatoxin-free diet. Broiler chicks one day old were distributed into five groups according to Saccharomyces cell wall and/or nanocurcumin with aflatoxin supplementation. The G1 group was given a formulated diet without any supplements. The G2 group was supplemented with aflatoxin (0.25 mg/kg diet) in the formulated diet. The G3 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1 kg/ton diet) in the formulated diet. The G4 group was supplemented with aflatoxin (0.25 mg/kg diet) and nanocurcumin (400 mg/kg) in the formulated diet. The G5 group was supplemented with aflatoxin (0.25 mg/kg diet) and Saccharomyces cell wall (1 kg/ton diet) in combination with nanocurcumin (200 mg/kg) in the formulated diet. RESULTS: According to the results of this study, aflatoxin supplementation had a detrimental impact on the growth performance, blood and serum parameters, carcass traits, and aflatoxin residue in the liver and muscle tissue of broilers. In addition, aflatoxin supplementation led to a liver injury that was indicated by serum biochemistry and pathological lesions in the liver tissue. Moreover, the shortening of villi length in aflatoxicated birds resulted in a decrease in both the crypt depth ratio and the villi length ratio. The expression of CYP1A1 and Nrf2 genes in the liver tissue increased and decreased, respectively, in the aflatoxicated group. In addition, the aflatoxin residue was significantly (P ≤ 0.05) decreased in the liver tissue of the aflatoxicated group after 2 weeks from the end of the experiment. CONCLUSION: Saccharomyces cell wall alone or with nanocurcumin attenuated these negative effects and anomalies and improved all of the above-mentioned metrics.

Nanocurcumin alleviates inflammation and oxidative stress in LPS-induced mastitis via activation of Nrf2 and suppressing TLR4-mediated NF-κB and HMGB1 signaling pathways in rats.

Coliform mastitis is a worldwide serious disease of the mammary gland. Curcumin is a pleiotropic polyphenol obtained from turmeric, but it is hydrophobic and rapidly eliminated from the body. However, nanoformulation of curcumin significantly improves its pharmacological activity by enhancing its hydrophobicity and oral bioavailability. Our study aimed to investigate the possible antioxidant and anti-inflammatory effects of nanocurcumin as a prophylactic against LPS-induced coliform mastitis in rat model, where LPS was extracted from a field strain of Escherichia coli (bovine mastitis isolate). The study was conducted on twenty lactating Wistar female rats divided into four equal groups, and the mastitis model was initiated by injection of LPS through the duct of the mammary gland. The results showed that nanocurcumin significantly attenuated the lipid peroxidation (MDA), oxidized glutathione, the release of pro-inflammatory cytokines (TNF-α and IL-1ß), and the gene expression of TLR4, NF-κB p65, and HMGB1. Meanwhile, it improved the reduced glutathione level and Nrf2 activity and preserved the normal alveolar architecture. These findings suggested that nanocurcumin supplementation can be a promising potential protective approach for coliform mastitis.

Commiphora myrrh Supplementation Protects and Cures Ethanol-Induced Oxidative Alterations of Gastric Ulceration in Rats.

Gastric ulceration is a multifactorial disease defined as a defect in the gastric wall that extends through the muscularis mucosae into the deeper layers of the wall. The most common cause of gastric ulceration is alcohol consumption. In the current study, rats were gavaged by ethanol to investigate the protective (before ethanol) and curative (after ethanol) ability of Commiphora myrrh (myrrh) oil and extract against gastric ulcer oxidative alterations induced by ethanol. Myrrh significantly improved ulcer index, histomorphology, and periodic acid Schiff (PAS) impaired by ethanol. In addition, myrrh improved the antioxidant potential of gastric mucosa through enhancement of nuclear factor related to erythroid 2 (Nrf2), total glutathione (GSH), reduced GSH, and oxidized glutathione (GSSG), along with significant reduction in malondialdehyde (MDA) levels. Amelioration of gastric oxidative stress by myrrh enables gastric mucosa to counteract the ethanol's inflammatory and apoptotic processes leading to improved gastric proliferation and healing. Interestingly, myrrh extract showed better protective and curative effects than myrrh oil against gastric ulceration.

The potential neuroprotective effect of allicin and melatonin in acrylamide-induced brain damage in rats.

Acrylamide (ACR) is an unsaturated monomer that served various fields; however, it is a potent neurotoxin. The target of the present study is to explore the neuroprotective efficacy of allicin and melatonin on ACR-induced neurotoxicity. Thirty-six male adult rats were non-selectively separated into six groups: placebo, allicin (20 mg/kg b.w daily per os), melatonin (10 mg/kg b.w 3 times/week per os), ACR (50 mg/kg b.w daily per os), ACR-allicin, and ACR-melatonin at the same doses as the preceding groups. The assessment of brain biomarkers, neurotransmitters, antioxidative status, Nrf2 signaling pathway, and histopathological analyses was performed following 21 days. ACR exposure induced brain lipid and DNA oxidative damage as well as reduced the glutathione (GSH) levels. The obvious brain oxidative injuries contributed to distinct brain dysfunction that was assured by alteration of brain neurotransmitters (serotonin, dopamine, acetylcholine, and acetylcholinesterase) and pathological brain lesions. Furthermore, ACR exposure increased hydroxy deoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), and amyloid protein (AB1-42). Finally, the mRNA transcripts of brain Keap-1, Nrf2, and NF-kB were upregulated after ACR intoxication. Interestingly, allicin and melatonin alleviated the ACR-induced brain damage assessed by the normalization of the mentioned analyses. The present study demonstrated the protective role of both allicin and melatonin in ACR-prompted neuropathy by alleviation of redox imbalance and enhancement of neurotransmitters as well as relieving DNA damage and anti-inflammatory effect.

Quercetin Attenuates Brain Oxidative Alterations Induced by Iron Oxide Nanoparticles in Rats.

Iron oxide nanoparticle (IONP) therapy has diverse health benefits but high doses or prolonged therapy might induce oxidative cellular injuries especially in the brain. Therefore, we conducted the current study to investigate the protective role of quercetin supplementation against the oxidative alterations induced in the brains of rats due to IONPs. Forty adult male albino rats were allocated into equal five groups; the control received a normal basal diet, the IONP group was intraperitoneally injected with IONPs of 50 mg/kg body weight (B.W.) and quercetin-treated groups had IONPs + Q25, IONPs + Q50 and IONPs + Q100 that were orally supplanted with quercetin by doses of 25, 50 and 100 mg quercetin/kg B.W. daily, respectively, administrated with the same dose of IONPs for 30 days. IONPs induced significant increases in malondialdehyde (MDA) and significantly decreased reduced glutathione (GSH) and oxidized glutathione (GSSG). Consequently, IONPs significantly induced severe brain tissue injuries due to the iron deposition leading to oxidative alterations with significant increases in brain creatine phosphokinase (CPK) and acetylcholinesterase (AChE). Furthermore, IONPs induced significant reductions in brain epinephrine, serotonin and melatonin with the downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and mitochondrial transcription factor A (mtTFA) mRNA expressions. IONPs induced apoptosis in the brain monitored by increases in caspase 3 and decreases in B-cell lymphoma 2 (Bcl2) expression levels. Quercetin supplementation notably defeated brain oxidative damages and in a dose-dependent manner. Therefore, quercetin supplementation during IONPs is highly recommended to gain the benefits of IONPs with fewer health hazards.

Effects of bovine lactoferrin and chitosan nanoparticles on serum biochemical indices, antioxidative enzymes, transcriptomic responses, and resistance of Nile tilapia against Aeromonas hydrophila.

The present study was carried out to investigate the effects of dietary bovine lactoferrin (BLF) or chitosan nanoparticles (CHN) alone or in combinations on serum biochemical indices, antioxidative capacity, transcriptomic responses, non-specific immunity, and resistance of Nile tilapia (Oreochromis niloticus) against challenge with Aeromonas hydrophila. Fish were fed on the basal diet with no supplements and served as control (CTR), and six other experimental diets containing different levels of BLF (800 and 1200 mg per kg diet), CHN (500 and 1000 mg per kg diet), and their combinations (400 mg BLF plus 250 mg CHN per kg diet, and 600 mg BLF plus 500 mg CHN per kg diet) for 45 days. At the end of the experiment, serum, and tissue specimens (liver and kidney) were collected, fish in all groups were challenged with A. hydrophila and then observed for another ten days to calculate the RPS. Compared to the CTR group, no significant differences were recorded in TP, ALB, GLO, BUN, and CREAT values among all treatments. Serum LYZ, ALT, AST, and ALP enzyme activities were significantly increased in all experimental groups over the CTR (P < 0.05), and their highest values were recorded in the combined treatments. Moreover, dietary supplementation with CHN (1000 mg/kg) and combined treatments significantly increased the SOD, CAT, and GSH-Px enzyme activities compared to other groups (P < 0.05). The highest mRNA expression levels of IGF-1 gene in liver, and IL-1ß, and IFN-γ genes in kidneys were found in CHN (1000 mg/kg) group and combined treatments more than other groups. Interestingly, no, or mild histopathological alterations were noticed in the hepatopancreas and posterior kidney of the treated groups. A significantly higher RPS was identified in the combined treatments challenged with A. hydrophila compared with the CTR group. This study exemplifies the positive impacts of dietary supplementation with BLF or CHN alone or combinations on the antioxidative status, immunity, and disease resistance of Nile tilapia.

Correction to: Ginkgo biloba mitigates silver nanoparticles-induced hepatotoxicity in Wistar rats via improvement of mitochondrial biogenesis and antioxidant status.

The original publication of this paper contains a mistake. The correct image of figure 3 is shown in this paper.

Ginkgo biloba mitigates silver nanoparticles-induced hepatotoxicity in Wistar rats via improvement of mitochondrial biogenesis and antioxidant status.

Silver nanoparticles (AgNPs) are noble metal nanoparticles, due to their good physicochemical properties, which have been exploited in biological applications. Nanotechnological applications advance very quickly while few literatures assessed the effects of natural products on the risks of nanoparticles in vivo. Thirty male adult rats were enrolled equally into: control, AgNPs (50 mg/kg b.w i.p 3 times/week) and GBE (100 mg/kg b.w daily per os)+AgNPs. After 30 days, the assessment of liver function, antioxidative status, mitochondrial biogenesis, and histopathological analyses were performed. AgNP exposure enhanced the hepatic lipid peroxidation (+ 281.7%) along with a decline in the reduced glutathione (- 58.3%) levels. The apparent hepatic oxidative damage was associated with obvious hepatic dysfunction that was ascertained by alteration of serum liver enzymatic biomarkers, lipid profile, and pathological hepatic lesions. Following AgNP exposure, hepatic silver and calcium contents were increased without changes in the trace element concentrations. Finally, the mRNA transcripts of hepatic PGC-1α, mtTFA, and Nrf2 were downregulated after AgNP exposure. Interestingly, GBE has the ability to alleviate AgNP-induced hepatic damage assessed by augmentation of reduced glutathione level and mitochondrial biogenesis. This study explored the potential protective role of GBE on AgNPs-induced hepatotoxicity via attenuation of oxidative stress, substantial enhancement of cell viability with concomitant mitigating DNA damage, and mitochondrial dysfunction.

Graviola attenuates DMBA-induced breast cancer possibly through augmenting apoptosis and antioxidant pathway and downregulating estrogen receptors.

Breast cancer is a global public health problem where it is the second most prevalent cancer. Historical cancer treatment with graviola has been reported. This study aimed to investigate the protective effects of graviola on 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat breast cancer. Fifty female Wistar rats were allocated into four groups: control group (gastro-gavaged by sesame oil), DMBA-treated group (gastro-gavaged a single dose of DMBA [50 mg/kg body mass, diluted in 1 ml sesame oil]) at the age 57 days, DMBA+G37-treated group (gastro-gavaged a single dose of DMBA [50 mg/kg body mass, diluted in 1 ml sesame oil]) at the age of 57 days plus graviola (200 mg/kg body mass) two times weekly (p.o.) at the age of 37 days till the end of the experiment, and DMBA+G57-treated group (received a single dose of DMBA [50 mg/kg body mass, diluted in 1 ml sesame oil]) plus graviola (200 mg/kg body mass) two times weekly at the age of 57 days until the end of the experiment. After the 30-week experimental period, blood samples were collected. Then, animals were sacrificed to determine the apoptotic indices, antioxidant status, and mammary gland tumor marker (CA 15-3). The DMBA upregulated the expression of one of the main anti-apoptotic genes: B-cell lymphoma protein 2 (BCL2) and estrogen receptor alpha (ER-α) gene. Moreover, it significantly increased breast lipid peroxidation and serum CA 15-3 but decreased breast antioxidant enzymatic activities (glutathione peroxidase, glutathione S-transferase, catalase, and superoxide dismutase). Nevertheless, administration of DMBA and graviola especially DMBA+G37 induced apoptosis through at least 1.5-fold in gene expression levels of pro-apoptotic genes: BCL2-associated X protein (BAX), tumor suppressor gene (P53), and cysteinyl-aspartic acid-protease-3 (caspase-3). A critical role of P53 in the regulation of the BCL2 and BAX has been reported. These proteins can determine if the cell undergoes apoptosis or cancels the process. Once the BAX gene activates caspase-3, there is no irreversible way toward cell death. Also, graviola ameliorated the DMBA effects on antioxidant enzymatic activities and tumor marker CA 15-3. This study concludes that graviola ameliorated DMBA-induced breast cancer potentially through upregulating apoptotic genes, downregulating the ER-α gene, increasing antioxidants, and decreasing lipid peroxidation levels.