Ameliorative effects of propolis and wheat germ oil on acute toxoplasmosis in experimentally infected mice are associated with reduction in parasite burden and restoration of histopathological changes in the brain, uterus, and kidney.

Toxoplasmosis continues to be a prevalent parasitic zoonosis with a global distribution. This disease is caused by an intracellular parasite known as Toxoplasma gondii, and the development of effective novel drug targets to combat it is imperative. There is limited information available on the potential advantages of wheat germ oil (WGO) and propolis, both individually and in combination, against the acute phase of toxoplasmosis. In this study, acute toxoplasmosis was induced in Swiss albino mice, followed by the treatment of infected animals with WGO and propolis, either separately or in combination. After 10 days of experimental infection and treatment, mice from all groups were sacrificed, and their brains, uteri, and kidneys were excised for histopathological assessment. Additionally, the average parasite load in the brain was determined through parasitological assessment, and quantification of the parasite was performed using Real-Time Polymerase Chain Reaction targeting gene amplification. Remarkably, the study found that treating infected animals with wheat germ oil and propolis significantly reduced the parasite load compared to the control group that was infected but not treated. Moreover, the group treated with a combination of wheat germ oil and propolis exhibited a markedly greater reduction in parasitic load compared to the other groups. Similarly, the combination treatment effectively restored the histopathological changes observed in the brain, uterus, and kidney, and the scoring of these reported lesions confirmed these findings. In summary, the present results reveal intriguing insights into the potential therapeutic benefits of wheat germ oil and propolis in the treatment of acute toxoplasmosis.

Mitigation of Hepatotoxicity via Boosting Antioxidants and Reducing Oxidative Stress and Inflammation in Carbendazim-Treated Rats Using Adiantum Capillus-Veneris L. Extract.

Exposure to food contaminants continues to be a substantial source of human health risks all over the world, particularly in developing countries. Carbendazim (CBZ) is a chemical fungicide used to control the spread of various fungi and other pathogens in the agriculture and veterinary sectors. The hazardous effects of CBZ on human health occur due to the accumulation of its residues in agricultural food products. In this study, the possible hepatoprotective effects of Adiantum capillus-veneris L. (ACVL) extract were evaluated in CBZ-treated rats. A GC-MS analysis revealed that ACVL extract contained several bioactive hydrocarbon components and fatty acids, and that the components exerted hepatic protection by mitigating oxidative stress via upregulating antioxidant agents and neutralizing nitrogen and oxygen free radicals. Moreover, ACVL extracts relieved hepatic inflammation via decreasing NO, NF-κB, and pro-inflammatory cytokines (TNF-a, IL-6) in the liver of CBZ-treated rats, both at protein and mRNA levels. In addition, the protective effect of ACVL has appeared in the histopathological figures and function markers in the livers of CBZ-treated rats. According to the present results, ACVL extract can protect the hepatic tissue and restore its functions to a control level in CBZ-treated rats; this effect may be attributed to its antioxidant and anti-inflammatory activities.

Therapeutic approaches for anti-sperm-antibodies in the testicular sperm aspiration rat model.

Background and Aim: Anti-sperm antibodies (ASAs) treatment continued to be neglected. This study aimed to generate ASAs using the testicular sperm aspiration (TSA) rat model, which allowed for investigation of four distinct therapeutic approaches to find potential treatments for ASAs. Materials and Methods: Adult Wistar albino male rats were divided into six equal groups (n = 12). The negative control group underwent scrotal sac surgery without having their testicles punctured. Punctures were made in the remaining 5 groups, with one group left untreated to serve as the positive control group. The remaining 4 groups were treated with either dexamethasone (DEX), azathioprine (AZA), frankincense, or anti-ASAs secondary antibodies. For 10 weeks, serum samples were collected every 2 weeks for specific quantification of ASAs. Testis and epididymis tissues were collected for histopathological analysis. Results: The ASAs concentrations of the positive controls were significantly higher (p ≤ 0.001) than their negative control counterparts during the examined weeks. However, The ASAs indices (%) differed according to the treatment type. While the ASAs indices at the 2nd and 4th weeks in the AZA-treated group were significantly reduced compared to the positive control group (p ≤ 0.001), no significant differences were observed at any of the sample collection week for the DEX-treated rats. The ASAs indices were significantly decreased only at weeks 6 and 8 of treatment in the frankincense-treated group (p ≤ 0.001). In the secondary antibodies-treated group, the antibody indices were significantly decreased in all weeks except for samples collected at week 4 (p ≤ 0.001). The testosterone levels reverted to normal only in TSA rats treated with either Frankincense or secondary antibodies, as they were significantly higher than the positive controls (p ≤ 0.05). Tissue samples from the secondary antibody-treated rats showed a generally normal histological appearance. Conclusion: This study tried to offer realistic therapy suggestions; however, caution should be applied when extrapolating findings from experimental models to meet clinical requirements.

Tamoxifen Increased Parasite Burden and Induced a Series of Histopathological and Immunohistochemical Changes During Chronic Toxoplasmosis in Experimentally Infected Mice.

The global distribution of breast cancer and the opportunistic nature of the parasite have resulted in many patients with breast cancer becoming infected with toxoplasmosis. However, very limited information is available about the potential effects of tamoxifen on chronic toxoplasmosis and its contribution to the reactivation of the latent infection. The present study investigated the potential effects of tamoxifen on chronic toxoplasmosis in animal models (Swiss albino mice). Following induction of chronic toxoplasmosis and treatment with the drug for 14 and 28 days, the anti-parasitic effects of tamoxifen were evaluated by parasitological assessment and counting of Toxoplasma cysts. In addition, the effects of the drug on the parasite load were evaluated and quantitated using TaqMan real-time quantitative PCR followed by investigation of the major histopathological changes and immunohistochemical findings. Interestingly, tamoxifen increased the parasite burden on animals treated with the drug during 14 and 28 days as compared with the control group. The quantification of the DNA concentrations of Toxoplasma P29 gene after the treatment with the drug revealed a higher parasite load in both treated groups vs. control groups. Furthermore, treatment with tamoxifen induced a series of histopathological and immunohistochemical changes in the kidney, liver, brain, and uterus, revealing the exacerbating effect of tamoxifen against chronic toxoplasmosis. These changes were represented by the presence of multiple T. gondii tissue cysts in the lumen of proximal convoluted tubules associated with complete necrosis in their lining epithelium of the kidney section. Meanwhile, liver tissue revealed multiple T. gondii tissue cysts in hepatic parenchyma which altered the structure of hepatocytes. Moreover, clusters of intracellular tachyzoites were observed in the lining epithelium of endometrium associated with severe endometrial necrosis and appeared as diffuse nuclear pyknosis combined with sever mononuclear cellular infiltration. Brain tissues experienced the presence of hemorrhages in pia mater and multiple T. gondii tissue cysts in brain tissue. The severity of the lesions was maximized by increasing the duration of treatment. Collectively, the study concluded novel findings in relation to the potential role of tamoxifen during chronic toxoplasmosis. These findings are very important for combating the disease, particularly in immunocompromised patients which could be life-threatening.

Immunohistochemical, histopathological, and biochemical studies of the NF-Ò¡B P65 marker in rat ovaries experimentally intoxicated by cadmium and the protective effect of the purslane plant extract.

The aim of this study is to describe the existence of the inflammatory marker nuclear factor kappa light chain B lymphocyte protein (NF-Ò¡B P65) in the tissue as a response to cadmium (CdCl2) toxicity. Next is to describe the disappearance of the NF-Ò¡B P65 in response to the purslane plant treatment to explore its anti-inflammatory effect, also describing the histopathological and biochemical changes that occurred from CdCl2 toxicity and the purslane plant tissue protections. There are four experimental groups, 32 rats (n = 8) intraperitoneally injected with CdCl2 and orally administered with purslane plant extract (according to groups) for 30 days: group one (control), group two (purslane extract 2 g/kg bw), group three (CdCl2 3.5 mg/kg bw), group four (CdCl2 3.5 mg/kg bw + purslane plant extract 2 g/kg bw). The biochemical findings showed that ovaries and brain tissue homogenates in group three showed malondialdehyde increase and reduction in catalase, total antioxidant capacity, and acetylcholine esterase. A reduction in serum LH, FSH, and estradiol were also recorded. These parameters became normal in group four. The histopathological findings exhibited that group three showed ovarian and cerebral hemorrhage and lung pneumonia. Tissues of group four were protected and no pathological lesions were detected. The immunohistochemical results showed that the inflammatory marker NF-Ò¡B P65 in group three was strongly detected in the spleen and moderately detected in the ovaries, brain, and lung but negatively detected in the tissues of group four. In conclusion, CdCl2 induced ovarian toxicity and the NF-Ò¡B P65 existence was increased. Purslane plant protected rats from CdCl2 toxicity and decrease NF-Ò¡B P65.

Adiantum capillus-veneris Linn protects female reproductive system against carbendazim toxicity in rats: immunohistochemical, histopathological, and pathophysiological studies.

This experimental study is done to clarify the protective role of the Adiantum capillus-veneris linn plant extracts (ACVL) in Sprague-Dawley female rat reproductive organs that are intoxicated by carbendazim pesticide (CBZ). This aim is achieved by the immunohistochemical detection of the inflammatory marker NF-Ò¡B-P65. This aim is achieved by the immunohistochemical detection of the inflammatory marker NF-Ò¡B-P65 and also, description of the histopathological and pathophysiological changes. Thirty-two rats were divided into four groups (n = 8) and were daily treated orally for 4 weeks. The first group as a control, the second group was treated with ACVL plant extract 200 mg/kg b.w., the third group was treated with CBZ 25 mg/kg b.w., and the fourth group was treated with CBZ 25 mg + ACVL plant extract 200 mg/kg b.w. The pathophysiological results showed that in the third group, the ovarian tissue malondialdehyde content was elevated, but the fourth group exhibited it at a normal level. Reductions in the ovarian tissue content of glutathione, superoxide dismutase activity, 3ß-hydroxysteroid dehydrogenase, 17ß-hydroxysteroid dehydrogenase, and also serum FSH, LH, and estradiol hormones were observed in the third group, while, in the fourth group, all these items recorded normal level. The histopathological findings in the third group exhibited severe congestion and hemorrhage in the ovaries, oviducts, myometrium, gastric submucosa, splenic white pulps, and brain subarachnoid spaces. The fourth group showed protection from the congestion and hemorrhage, and no histopathological changes occurred. The immunohistochemical results in the third group revealed strong positive immunoreaction against the NF-Ò¡B-P65 antigen in the uterus and stomach. Ovaries, spleen, and brain showed moderate positive immunoreaction. The fourth group disclosed negative immunoreaction for the NF-Ò¡B-P65 antigen. In conclusion, CBZ toxicity induced histopathological changes in female rat reproductive organs. CBZ induced changes in the enzymatic activities measured in ovarian and brain tissue homogenates. CBZ causes an elevation in NF-Ò¡B P65 as an inflammatory marker, especially in the uterus and stomach. The ACVL plant extract acts as a protective factor to prevent the CBZ toxicity and also has an anti-inflammatory effect by decreasing the synthesis of NF-Ò¡B-P65.

Antiulcerogenic effect of Cuphea ignea extract against ethanol-induced gastric ulcer in rats.

BACKGROUND: Cuphea ignea is one of the herbal resources belonging to Lythraceae family. Some species of this family have been used traditionally in South and Central America's folk medicine for treating stomach disorders. Therefore, the present study was performed to evaluate the gastropreventive effect of aqueous ethanolic extract of C. ignea aerial parts on ethanol-induced gastric ulcer. METHODS: Gastric ulcers were induced in Sprague Dawley rats using one oral dose of absolute ethanol (1.5 mL/rat). The C. ignea aerial parts extract at doses of 250 and 500 mg/kg body weight and ranitidine (a reference drug) at a dose of 30 mg/kg body weight were orally administrated daily for 7 days before ulcer induction. One hour after ethanol administration blood samples were collected and then stomachs of sacrificed rats were subjected to biochemical, macroscopic and microscopic studies. RESULTS: Oral administration of C. ignea extract significantly attenuated gastric ulcer as revealed by significant reduction in the gastric ulcer index and volume of gastric juice while significantly increased preventive percentage, gastric pH value and pepsin activity. Pre-treatment of C. ignea extract markedly improved the serum level of TNF-α, the gastric MPO activity and NO content. Furthermore, C. ignea pre-treatment significantly increased the gastric levels of enzymatic and non- enzymatic antioxidants namely CAT, SOD, GSH-Px, and GSH with concomitant reduction in MDA level compared with those in the ethanol group. These results were further supported by histopathological findings which revealed the curing effect of C. ignea on the hemorrhagic shock induced by ethanol toxicity. CONCLUSIONS: C. ignea extract showed a potential gastroprotective effect on ethanol-induced gastric ulcer, and its effect may be mediated through suppression of oxidative stress and gastric inflammation.