Evaluation of the Protective Effect of Olive Leaf Extract on Cisplatin-Induced Testicular Damage in Rats

In the present investigation, the effect of olive leaf extract (OLE) on testicular damage induced in rats by an intraperitoneal injection of cisplatin (cis-diamminedichloroplatinum (CDDP)) at a dose of 5 mg/kg was tested. Rats were randomly divided into 4 groups: control, CDDP, OLE, and OLE + CDDP. After 5 days of CDDP treatment, body and testicular weights, histopathological alteration, and serum male sex hormone levels were determined. In addition to the biochemical and immunohistochemical changes in the testes, CDDP caused the disorganization of germinal epithelium and apoptosis by inducing Bax and inhibiting Bcl-2 protein expression. Testicular weights, catalase, serum testosterone, testicular enzymatic (including glutathione peroxidase, glutathione reductase, and superoxide dismutase) along with nonenzymatic (glutathione) antioxidants, and levels of luteinizing and follicle-stimulating hormones were significantly reduced in addition to a significant increase in testicular malondialdehyde and nitrite/nitrate levels when compared with the control group. OLE treatment markedly attenuated both biochemical and histopathological changes. The reproductive beneficial effects of OLE were mediated, at least partly, by inducing the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway

Role of reactive oxygen species: In the cytotoxicity and apoptosis of colon cancer cell line due to green lead nanoparticles

Nanoparticles are involved in regulating the biology of cancer cell treatment, but their mechanism is not fully understood. We synthesized and characterized new green lead nanoparticles (gPbNPs) by using an extract of Ziziphus spina christi leaves. Its cytotoxic and apoptotic effect on the human colon cancer Cacoa2 cell line was evaluated. The gPbNPs were characterized by using energy dispersive X-rays, scanning electron microscopes, and transmission electron microscopes. The cytotoxic effects of gPbNPs against the human colon cancer Cacoa2 cell line were investigated, as were the possible mechanisms underlying the induction of apoptosis. In this experiment, we observed the production of intracellular reactive oxygen species (ROS) in cells, and the installation of caspase 3/7 was higher in cells at 16 µg/mL of gPbNPs. Moreover, the Bax gene was upregulated and the Bcl2 gene was downregulated, and increased caspase-3/7 activity confirmed the apoptotic effect of gPbNPs in cells. The cytotoxicity test confirmed that gPbNPs were selectively toxic in cancer cells and induced apoptosis by activating bad, bax, caspase-3/7, p27, p53 protein, and proteins involved in apoptosis. Our observation showed that gPbNPs induced cell toxicity, increased generation of intracellular ROS, and gene expression of Bcl2, and Bax, in the Cacoa2 cell line. In conclusion, these findings demonstrated that gPbNPs executed toxic effects on the Cacoa2 cell line by activating caspase-3/7 activity

Ziziphus spina-christi leaf extract ameliorates schistosomiasis liver granuloma, fibrosis, and oxidative stress through downregulation of fibrinogenic signaling in mice.

Schistosomiasis is a widespread parasitic infection that affects humans, as well as wild and domestic animals. It ranks second after malaria, with a significant health and socio-economic impact in the developing countries. The objective of this study was to assess the anti-schistosomal impact of Ziziphus spina-christi leaf extract (ZLE) on Schistosoma mansoni-induced liver fibrosis in CD-1 Swiss male albino mice. S. mansoni infection was achieved by dipping of mouse tails in schistosomal cercariae. ZLE treatment was initiated at 46 days post-infection by administering a dose of the extract on a daily basis for 10 consecutive days. S. mansoni infection resulted in liver granuloma and fibrosis, with a drastic elevation in liver function factors, nitric oxide, and lipid peroxidation, which were associated with a reduction in glutathione content and substantial inhibition of antioxidant enzyme activities compared to those of the control. Induction of hepatic granuloma, oxidative stress, and fibrosis in the liver was controlled by ZLE administration, which also produced inhibition of matrix metalloproteinase-9, alpha-smooth muscle actin, transforming growth factor-β, and tissue inhibitors of metalloproteinases expressions. In addition, the S. mansoni-infected group exhibited an increase in Bax and caspase-3 levels and a decrease in Bcl-2 level. However, treatment with ZLE mainly mitigated apoptosis in the liver. Thus, the findings of this study revealed that Ziziphus spina-christi had anti-apoptotic, anti-fibrotic, antioxidant, and protective effects on S. mansoni-induced liver wounds. The benefits of Ziziphus spina-christi extract on S. mansoni were partly partially mediated by enhancing anti-fibrinogenic and nuclear factor erythroid 2-related factor 2 (Nrf2) pathways

Antifungal Potential of Aqueous Extract of Boswellia carteri

To assess the antifungal activity of the crude aqueous extract of B. carteri. Three independent concentrations (1%, 2.5%, and 5%) of the crude aqueous extract of B. carteri were tested for their in vitro activity against selected fungal strains. The treated (5% concentration) and untreated A. alternata samples were analyzed for morphological changes using scanning electron microscopy (SEM). Fourier-Transform Infrared (FTIR) spectrometry of the extract was done to identify the phytoconstituents responsible for the antifungal activity. Results showed that the crude aqueous extract of B. carteri inhibited the growth of all the selected fungal species. The percentage of mycelial growth of the tested fungi decreased as the concentration of the aqueous extract increased from 1% to 5%. SEM-based studies of A. alternata treated with 5% showed significant morphological changes including shrunken hyphae, membrane disintegration, and distorted conidial structures compared to the untreated fungal cells. The crude aqueous extract of B. carteri has the potential to be used as a natural and effective fungicidal agent for controlling the growth of pathogenic fungi

Ameliorative Effect of Beta vulgaris Root Extract on Chlorpyrifos-Induced Oxidative Stress, Inflammation and Liver Injury in Rats

Exposure to organophosphorus insecticides causes several health problems to animals and humans. Red beetroot (RBR) is rich in antioxidant ingredients and possesses a promising hepatoprotective activity. This study evaluated the potential of RBR extract to prevent chlorpyrifos (CPF)-induced liver injury, with an emphasis on oxidative stress, inflammation and apoptosis. Rats received 10 mg/kg CPF and were treated with 300 mg/kg RBR extract for 28 days. CPF caused liver injury evidenced by elevated serum levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and bilirubin, along with several histological alterations. Hepatic lipid peroxidation (LPO) and nitric oxide (NO) levels, as well as inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines were increased in CPF-intoxicated rats. RBR prevented CPF-induced histological alterations, and ameliorated liver function, LPO, NO, iNOS and pro-inflammatory cytokines. RBR boosted glutathione and antioxidant enzymes, and increased Nrf2 expression. In addition, RBR diminished Bax and caspase-3, and increased Bcl-2 expression. In conclusion, RBR prevented CPF-induced liver injury via attenuation of oxidative stress, inflammation and apoptosis. RBR enhanced antioxidant defenses, suggesting that it could be used as a potential therapeutic intervention to minimize CPF hepatotoxicity

Red Beetroot Extract Abrogates Chlorpyrifos-Induced Cortical Damage in Rats

Organophosphorus insecticides including chlorpyrifos (CPF) are mainly used for agriculture, household, and military purposes; their application is associated with various adverse reactions in animals and humans. This study was conducted to evaluate the potential neuroprotective effect of red beetroot methanolic extract (RBR) against CPF-induced cortical damage. Twenty-eight adult male Wistar albino rats were divided into 4 groups (n=7 in each group): the control group was administered physiological saline (0.9% NaCl), the CPF group was administered CPF (10 mg/kg), the RBR group was administered RBR (300 mg/kg), and the RBR+CPF group was treated with RBR (300 mg/kg) 1 hr before CPF (10 mg/kg) supplementation. All groups were treated for 28 days. Rats exposed to CPF exhibited a significant decrease in cortical acetylcholinesterase activity and brain-derived neurotrophic factor and a decrease in glial fibrillary acidic protein. CPF intoxication increased lipid peroxidation, inducible nitric oxide synthase expression, and nitric oxide production. This was accompanied by a decrease in glutathione content and in the activities of glutathione peroxidase, glutathione reductase, superoxide dismutase, and catalase in the cortical tissue. Additionally, CPF enhanced inflammatory response, indicated by increased levels and expression of interleukin-1β and tumor necrosis factor-α. CPF triggered neuronal apoptosis by upregulating Bax and caspase-3 and downregulating Bcl-2. However, RBR reversed the induced neuronal alterations following CPF intoxication. Our findings suggest that RBR can minimize and prevent CPF neurotoxicity through its antioxidant, anti-inflammatory, and antiapoptotic activities