The Potential Gastro-Protective Effect of Qaysum (Achillea fragrantissima) Against Ethanol-Induced Gastric Ulcer in Wistar Albino Rats.

Gastric ulcer (GU) is among the peak prevalent syndromes. This study investigates the defensive properties of Achillea fragrantissima (Forssk.) Sch.Bip. extract (AFE) against ethanol-induced stomach lesions. Twenty-eight rats were allocated into negative control, positive control, AFE + ethanol, and omeprazole ethanol. In serum and gastric homogenates, oxidative stress displays (e.g., malondialdehyde (MDA), decreased glutathione (GSH), superoxide dismutase enzyme (SOD), and catalase enzyme (CAT)) and inflammatory parameters (e.g., tumor necrosis factor-alpha (TNF-α)) were estimated. GU markers (gastric lesions, ulcer index (UI), pH) were evaluated, and gastric histopathological examinations were performed. The positive control cluster exhibited severe gastric mucosal injuries, reduced stomach mucus secretion, and pH of gastric content. Furthermore, AFE-pretreated rats displayed meaningfully increased periodic acid-Schiff (PAS) countenance in their stomach epithelial layers. Pretreatment with AFE reduced stomach lesions, UI, MDA, and TNF-α levels, while mucus, pH, CAT, GSH, and SOD levels increased. Stomach examination showed significant improvement in gastric mucosa reduced edema and leukocyte infiltration of the submucosal level in pretreatment with the AFE and omeprazole groups versus the ethanol group. Additionally, AFE extracts increase the intensity of the stomach epithelium's PAS. The acute toxicity experiment with an advanced dosage of 5 g/kg AFE did not exhibit any signs of toxicity in the rats. In conclusion, the AFE reduced the effect of ethanol on the gastric mucosa, which may be due to its antioxidants and anti-inflammatory properties.

Punicalagin Protects against the Development of Methotrexate-Induced Hepatotoxicity in Mice via Activating Nrf2 Signaling and Decreasing Oxidative Stress, Inflammation, and Cell Death.

Despite its effectiveness in treating inflammatory diseases and various malignancies, methotrexate (MTX) is well known to cause hepatotoxicity, which involves increased oxidative stress and inflammation, limiting its clinical use. Herein, we looked into the effect of punicalagin (PU), a polyphenolic molecule having a variety of health-promoting attributes, on MTX-induced hepatotoxicity in mice. PU (25 and 50 mg/kg/day) was given orally to the mice for 10 days, while a single dose of MTX (20 mg/kg) was injected intraperitoneally (i.p.) at day 7. The MTX-induced liver damage was demonstrated by remarkably higher transaminases (ALT and AST), ALP, and LDH, as well as significant histological alterations in hepatic tissues. MTX-injected mice also demonstrated increases in hepatic oxidative stress markers, including malondialdehyde (MDA) and nitric oxide (NO), with a concordant drop in glutathione (GSH) content and superoxide dismutase (SOD) and catalase (CAT) activities. PU significantly attenuated the MTX-induced serum transaminases, ALP and LDH elevations, and hepatic oxidative stress measures and boosted antioxidant defenses in the liver. Moreover, the liver of MTX-treated mice showed increases in NF-κB p65 expression, pro-inflammatory cytokine (IL-6 and TNF-α) levels, and pro-apoptotic protein (caspase-3 and Bax) expression, whereas Bcl-2 and Nrf2 expressions were reduced, which were all attenuated by PU treatment. Collectively, PU inhibits oxidative damage, inflammation, and apoptosis and upregulates Nrf2 in the liver of MTX-induced mice. Thus, these findings suggest that PU may have great therapeutic potential for the prevention of MTX-induced hepatotoxicity, pending further exploration in upcoming studies.

Impacts of sex steroids and aromatase inhibitor on performances, carcass characteristics and gonadal histology of broiler chickens slaughtered at different ages.

This experiment was established to evaluate the influence of synthetic steroid hormone and aromatase inhibitor on performance, carcass characteristics, hormonal profile and gonadal structure of broiler chickens slaughtered at two different ages. A total of 360 Cobb Avian48 chicks were sexed and distributed randomly into three groups: Tam10 group; birds received Tamoxifen10mg (Tamfen 10 mg@ ) orally at a level of 10 mg/kg body weight daily from the 3rd till the 9th day of age; BOL group: birds injected intramuscularly with Boldenone undecylenate (BOLD-GAN@ 0.1 mg/kg) at the 5th and the 9th day of age; and Control group. BOL injection or Tam supplementation improved performance traits compared with the control group. Although Tam positive effect appeared early before the 5th week of age, the BOL effect was delayed to the 6th week. BOL injection improved carcass characteristics of both sexes at both 5 and 6 weeks slaughtering ages. Regardless of treatment effect, the mortality% was higher in the late weeks of age than in the early weeks. Moreover, BOL treatment increased comb% compared with control and Tam treatments. Generally, males had significantly higher testosterone levels and lower oestrogen levels than females. Males treated with Boldenone had the highest testosterone level, although testosterone levels did not differ considerably among females of the various groups. BOL treatment females had the lowest oestrogen level. Both Tam10 and Boldenone had adverse effects on testicular and ovarian histology, affecting the typical structures. Finally, we concluded that the anabolic effect of Tam10 may be achieved in griller broilers production without changing the sex hormones assay. Although Boldenone achieved an anabolic effect without changing blood sex hormone levels, this effect is induced early with females and delayed with males, which prolongs the marketing period. The goal is to shorten this period. Therefore, this material can only be used with the possibility of separating females from males to be used with females only.

Antitumor Activity of Royal Jelly and Its Cellular Mechanisms against Ehrlich Solid Tumor in Mice.

Objective: The present study was aimed at evaluating the antitumor effects of royal jelly (RJ) obtained from Apis mellifera compared with cyclophosphamide against the Ehrlich solid tumors (EST) in mice. Methods: Tumor growth inhibition, body weight, the serum level of alpha-fetoprotein (AFP) and carcinoembryonic antigen tumor (CAE), liver and kidney enzymes, tumor lipid peroxidation (LPO), nitric oxide (NO), antioxidant enzymes (glutathione peroxidase (GPx), catalase enzyme (CAT), and superoxide dismutase enzyme activity (SOD)), tumor necrosis factor alpha level (TNF-α), and the apoptosis-regulatory genes expression were assessed in EST mice treated with RJ (200 and 400 mg/kg orally once a day for 2 weeks). Results: The results showed that treatment of EST-suffering mice with RJ at the doses of 200 and 400 mg/kg causes significant reduction in tumor volume and inhibition rate, body weight, tumor markers (AFP and CEA), serum level of liver and kidney, LPO and NO, TNF-α level, as well as the expression level of Bcl-2 in comparison with the EST mice receiving the normal saline; whereas RJ at the doses of 200 and 400 mg/kg/day significantly increased (p < 0.05) the level of antioxidant enzymes of GPx, CAT, and SOD and the expression level of caspase-3 and Bax genes. Conclusion: The findings revealed that oral administration of royal jelly especially at the doses of 200 and 400 mg/kg exhibited promising antitumor effects against EST in mice through induction of apoptosis as well as its antioxidant and anti-inflammatory effects, which suggest it as a novel anticancer agent against tumor; however, additional surveys especially in clinical setting are necessary to approve these findings.

Anti-Tumor Effects of Queen Bee Acid (10-Hydroxy-2-Decenoic Acid) Alone and in Combination with Cyclophosphamide and Its Cellular Mechanisms against Ehrlich Solid Tumor in Mice.

Queen bee acid or 10-hydroxy-2-decenoic acid (10-HDA) is one of the main and unique lipid components (fatty acids) in royal jelly. Previous studies have demonstrated that 10-HDA has various pharmacological and biological activities. The present study aims to evaluate the anti-tumor effects of 10-HDA alone and combined with cyclophosphamide (CP), as an alkylating agent which widely used for the treatment of neoplastic cancers, against the Ehrlich solid tumors (EST) in mice. Methods: A total of 72 female Swiss albino mice were divided into eight groups. EST mice were treated with 10-HDA (2.5 and 5 mg/kg) alone and combined with CP (25 mg/kg) orally once a day for 2 weeks. Tumor growth inhibition, body weight, the serum level of alpha-fetoprotein (AFP) and carcinoembryonic antigen tumor (CAE), liver and kidney enzymes, tumor lipid peroxidation (LPO) and nitric oxide (NO), antioxidant enzymes (e.g. glutathione reductase (GR), glutathione peroxidase (GPx), catalase enzyme (CAT)), tumor necrosis factor alpha level (TNF-α), and the apoptosis-regulatory genes expression were assessed in tested mice. Results: the findings exhibited that treatment of EST-suffering mice with 10-HDA at the doses of 2.5 and 5 mg/kg especially in combination with CP significantly (p < 0.001) decreased the tumor volume and inhibition rate, tumor markers (AFP and CEA), serum level of liver and kidney, LPO and NO, TNF-α level, as well as the expression level of Bcl-2 in comparison with the mice in the C2 group; while 10-HDA at the doses of 2.5 and 5 mg/kg especially in combination with CP significantly (p < 0.001) improved the level of antioxidant enzymes of GPx, CAT, and SOD and the expression level of caspase-3 and Bax genes. Conclusions: According to the results of the present investigations, 10-HDA at the doses of 2.5 and 5 mg/kg especially in combination with CP showed promising antitumor effects against EST in mice and can be recommended as a new or alternative anticancer agent against tumor; nevertheless, further investigations, particularly in clinical setting, are required to confirm these results.