The mollifying effect of Sambucus nigra extract on StAR gene expression, oxidative stress, and apoptosis induced by fenpropathrin in male rats.

Fenpropathrin (FNP) is a man-made insecticide of to the pyrethroid class, commonly employed in agricultural and horticultural practices. However, it has a prolonged persistence in the environment. Sambucus nigra, also referred to as SN, is a botanical species recognized for its notable antioxidant characteristics. The objective of this study was to examine if SN extract could mitigate the reproductive toxicity induced by FNP in rats. A total of thirty rats were categorized into six distinct groups: a control group with no treatment, two groups getting SN extract at varying doses, a group receiving FNP, and two groups receiving both FNP and SN extract. The exposure to FNP led to a decline in the number and movement of sperm, lowered levels of testosterone, and reduced the activity of the StAR gene in the FNP group compared to the control group (p < 0.05). In addition, FNP resulted in a significant increase in malondialdehyde levels with a significant drop in GSH content compared to the control group (p < 0.05). Also, a significant increase in the expression of caspase 3. Nevertheless, the administration of SN extract alleviated these effects and reinstated spermatogenesis, thereby bringing the parameters closer to those observed in the control group. The data indicate that FNP can induce testicular harm and infertility, but SN extract can mitigate these detrimental consequences.

The Reproductive Injury and Oxidative Testicular Toxicity Induced by Chlorpyrifos Can Be Restored by Zinc in Male Rats.

The current study aimed to evaluate the harmful effect of chlorpyrifos (CPF) on the reproductive functions and fertility in male rats and to assess the protective role of zinc (Zn) in improving the adverse effects of CPF on male fertility. Sixty mature male rats were divided into four groups: Group 1: The control group was orally administered with the corresponding dose of corn oil. Group 2 animals received chlorpyrifos (1 mg/kg, oral). Group 3 rats received oral zinc (25 mg/kg) daily. Group 4 animals received oral zinc treatment (25 mg/kg). CPF caused a significant decrease in the body and reproductive organs' weights, sperm count, sperm motility percent, serum testosterone, FSH, and LH. The CPF-treated group showed a significant increase in dead sperm percent and sperm abnormalities. CPF induced a significant internucleosomal DNA fragmentation and marked histological alterations in the testes of treated male rats. Conversely, co-treatment with Zn improved the reproductive organs weights, sperm characteristics, internucleosomal DNA fragmentation, and histological alterations of the testes. In conclusion, CPF triggered significant detrimental effects on male reproductive organs and functions and the co-treatment with zinc partly alleviate the injurious effects of CPF on male fertility.

Lucrative antioxidant effect of metformin against cyclophosphamide induced nephrotoxicity.

Cyclophosphamide is anticancer drug with a well-Known nephrotoxicity. This work was applied to study the lucrative antioxidant influence of metformin as co-therapy on the nephrotoxicity induced by cyclophosphamide in the treatment of different cancer diseases. Four groups of male Sprague Dawley rats were used; Control group (C) received single I.P. injection of 0.2 ml saline, Metformin (MET) group received daily gavage of 200 mg/kg metformin for two weeks, Cyclophosphamide (CP) group received single I.P. injection of 200 mg/kg CP, Protector group (CP.MET) received daily gavage of 200 mg/kg metformin for two weeks and single I.P. injection of 200 mg/kg CP at day 7. By day 14 rats were euthanized. Samples were collected from kidney tissues and blood for kidney function evaluation, histopathological and assessment of oxidative stress markers. The results disclosed that CP yields many functional and structural damage to the kidney, worsened oxidative stress markers and kidney function indicators. The protector group displayed better kidney tissue morphology, acceptable kidney function indicators as well as satisfactory oxidative stress markers. In assumption, metformin could be combined with CP owing to its lucrative effect counter to CP persuaded nephrotoxicity.

Rosmarinic acid attenuates chromium-induced hepatic and renal oxidative damage and DNA damage in rats.

Hexavelant chromium (Cr (V1)) is a widely distributed environmental pollutant inducing damage in different organs of human and animals. The current study was designed to investigate the mechanistic role of rosmarinic acid (RA) to diminish chromium-induced hepatorenal oxidative damage and preneoplastic lesions in rats. Plant material was collected, identified, and extracted. The isolated RA was elucidated relying on the nuclear magnetic resonance spectroscopic data. Twenty-eight male Wistar rats received the following materials daily via oral gavage for 60 days; (Gp1): normal saline, (Gp2) 25 mg/kg.bwt RA, (Gp3) 10 mg/kg.bwt potassium dichromate (K2 Cr2 O7 ), (Gp4) K2 Cr2 O7 + RA. All rats were euthanized at the end of the experiment by cervical dislocation and the liver and kidney were collected. Prolonged continuous exposure of rats to chromium-induced oxidant/antioxidant imbalance manifested by significant elevation of malondialdehyde with reduction in reduced glutathione levels. Remarkable histopathological alterations in the liver and kidney tissue sections were recorded and confirmed by overexpression of the immunohistochemical staining of caspase-3, placental glutathione-S transferase, proliferating cell nuclear antigen together with a significant downregulation of nuclear factor erythroid-2 related factor 2 (Nrf2) gene and upregulation of nibrin gene. Observable improvements in the entire toxicopathological parameters were recorded in group cotreated with RA. Our findings revealed that Cr-induced preneoplastic lesions on the liver and kidney tissues of rats when exposed daily for long period of time, as well as confirmed the ability of RA to alleviate this toxicity through upregulation of Nrf2 pathway and its powerful antioxidant effects.

Testicular Caspase-3 and ß-Catenin Regulators Predicted via Comparative Metabolomics and Docking Studies.

Many routes have been explored to search for effective, safe, and affordable alternatives to hazardous female contraceptives. Herbal extracts and their secondary metabolites are some of the interesting research areas to address this growing issue. This study aims to investigate the effects of ten different plant extracts on testicular spermatogenesis. The correlation between the chemical profile of these extracts and their in vivo effect on male reproductive system was evaluated using various techniques. Approximately 10% of LD50 of hydro-methanolic extracts were orally administrated to rats for 60 days. Semen parameters, sexual organ weights, and serum levels of male sex hormones in addition to testes histopathology, were evaluated. Moreover, metabolomic analysis using (LC-HRESIMS), multivariate analysis (PCA), immunohistochemistry (caspase-3 and ß-catenin), and a docking study were performed. Results indicated that three plant extracts significantly decreased epididymal sperm density and motility. Moreover, their effects on testicular cells were also assured by histopathological evaluations. Metabolomic profiling of the bioactive plant extracts showed the presence of diverse phytochemicals, mostly oleanane saponins, phenolic diterpenes, and lupane triterpenes. A docking study on caspase-3 enzyme showed that oleanane saponins possessed the highest binding affinity. An immunohistochemistry assay on ß-catenin and caspase-3 indicated that Albizzia lebbeck was the most active extract for decreasing immunoexpression of ß-catenin, while Rosmarinus officinalis showed the highest activity for increasing immunoexpression of caspase-3. The spermatogenesis decreasing the activity of A. lebbeck, Anagallis arvensis, and R. officinalis can be mediated via up-regulation of caspase-3 and down-regulation of ß-catenin existing in testis cells.

Histopathological, immunohistochemical, and molecular studies for determination of wound age and vitality in rats.

In forensic medicine, it is vital to verify with the best attainable accuracy once injuries occurred during vital or post-mortem conditions. An immunohistochemical study was carried out to examine the time-dependent expression of macrophage-specific gene CD68 (cluster of differentiation 68), alpha-smooth muscle actin (α-SMA), and vascular endothelial growth factor (VEGF) in different skin wound timings (0, 1, 3, 5, 7, and 14 days) in rats. Histopathological studies were performed to assess the wound age and vitality. Eighteen male albino Wister rats (weighing 170-200 g) were used for wound induction. Rats (n = 3) were euthanised at 0, 1, 3, 5, 7, and 14 days from the starting point of wound induction. Histopathological examination showed that the epidermal re-epithelialisation was completed 14 days after skin incision. The inflammatory phase was recorded during the first 3 days of healing and reached the maximum levels at 5 days, then declined after 7 days, and completely removed at 14 days. The beginning of the proliferative phase was dated to day 3 and the peak at days 5 and 7. The initiation of the granulation tissue formation and remodelling phase of the healing process was observed 5 days after wounding. By immunohistochemical staining, negative VEGF gene expressions at early stages (0-3 days) were observed, as well as neither CD68+ macrophages nor α-SMA+ myofibroblast cells were detected. By increasing the wound ages (5-7 days), granulation tissue and angiogenesis were observed, with the migration of macrophages and fibroblast, which expressed VEGF, CD68, and α-SMA positive reaction. Time-dependent expression of the above markers suggested that they would be useful indicators for the determination of wound age. Both VEGF and transforming growth factor-beta 1 (TGFb1) mRNA levels were determined in different skin wound ages. The transcription of TGFb1 and VEGF increased shortly after wounding, until post-wounding day 7. It then declined constantly, reaching minimal values on day 14.

Metabolic profile and hepatoprotective effect of Aeschynomene elaphroxylon (Guill. & Perr.).

Liver diseases are life-threatening and need urgent medical treatments. Conventional treatment is expensive and toxic, so the urge for nutraceutical hepatoprotective agents is crucial. This study is considered the first metabolic profile of Aeschynomene elaphroxylon (Guill. & Perr.) extracts of; flowers, leaves & bark adopting UPLC-Orbitrap HRMS analysis to determine their bioactive metabolites, and it was designed to investigate the potential hepatoprotective activity of A. elaphroxylon flowers and bark extracts against CCl4-induced hepatic fibrosis in rats. Forty-nine compounds of various classes were detected in the three extracts, with triterpenoid saponins as the major detected metabolite. Flowers and bark extracts presented similar chemical profile while leaves extract was quite different. The antioxidant activities of the flowers, leaves & bark extracts were measured by in vitro assays as Fe+3 reducing antioxidant power and Oxygen radical absorbance capacity. It revealed that flowers and bark extracts had relatively high antioxidant activity as compared to leaves extract. Based on the metabolic profile and in vitro antioxidant activity, flowers and bark ethanolic extracts were chosen for alleviation of hepatotoxicity induced by CCl4 in rats. The hepatoprotective activity was studied through measuring hepatotoxicity biomarkers in serum (ALT, AST, and Albumin). Liver tissues were examined histopathologically and their homogenates were used in determining the intracellular levels of oxidative stress biomarkers (MDA, GSH), inflammatory markers (TNF-α). Flowers and bark ethanolic extracts exerted a significant hepatoprotective effect through reduction in the activities of ALT, AST and Albumin, the tested extracts reduced oxidative stress by increasing GSH content and reducing the MDA level. Furthermore, the extracts decreased levels of pro-inflammatory TNF-α. Moreover, the present study revealed the potentiality of A. elaphroxylon in ameliorating the CCl4-induced hepatic fibrosis in rats. In this aspect, A. elaphroxylon can be used with other agents as a complementary drug.