Thiazole and its derivatives have received a lot of attention from researchers due to its wide biological, pharmacological, and anticancer properties. A novel series of 2-[2-[4-Hydroxy-3-substituted benzylidene hydrazinyl]-thiazole-4[5H]-ones (4a–c) and acetoxy derivative (5) were synthesized via using thiosemicarbazones (2a–c). The structure of the thiazole derivatives (4a–c) and 5 in these compounds was confirmed by spectroscopic techniques (IR and NMR), as well as elemental investigations. The synthesized derivatives biological activity was assessed based on their capacity to suppress the growth of the cancer cell lines MCF-7 and HepG2, as well as to halt the cell cycle and trigger apoptosis. Among the synthesized thiazole derivatives, compound 4c was found the most active derivative, with inhibitory concentrations IC₅₀ = 2.57 ± 0.16 and 7.26 ± 0.44 µM in MCF-7 and HepG2, respectively, compared to Staurosporine as the standard drug with IC₅₀ 6.77 ± 0.41 and 8.4 ± 0.51 µM, respectively. Additionally, compound 4c blocked vesicular endothelial growth factor receptor-2 (VEGFR-2), according to our results (IC₅₀ = 0.15 µM), compared to Sorafenib (IC₅₀ = 0.059 µM) as the standard drug. Moreover, compound 4c induced cell cycle arrest at the G1/S phase, increasing the percentage and accumulation of cancer cells (DNA content) in the pre-G1 phase by 37.36% in MCF-7 cancer cells compared to untreated MCF-7 cells at 2.02%. Also, compound 4c increased the percentage of early and late apoptosis from 0.51% and 0.29%, respectively, in the case of the MCF-7 untreated control sample to 22.39% and 9.51%, respectively, in the MCF-7 treated sample. Furthermore, molecular docking studies of compounds 4a–c and 5 were conducted with four key proteins (aromatase, epidermal growth factor receptor (EGFR), cyclin-dependent kinase 2 (CDK2), and B-cell lymphoma 2 (Bcl-2)) that stimulate the growth, proliferation, and development of cancer cells. Compound 4c exhibited good docking scores with a promising and potential binding affinity toward the active site of selected docked proteins. According to these results, compound 4c showed efficient cytotoxic activity against the tested cancer cells.

Thioacetamide (TAA) was administered to induce an animal model of liver disease with secondary splenomegaly to assess the mechanisms underlying the effects of rapamycin and filgrastim when taken separately or in combination on the biochemical and histopathological aspects of the liver and spleen. Thirty adult male albino rats were divided into five groups (control, TAA-treated group, TAA+rapamycin, TAA+filgrastim, and TAA+rapamycin+filgrastim group). We measured relative liver and spleen weights, serum levels of alanine transaminase (ALT), aspartate transaminase (AST), and albumin. Molecular docking modeling and histopathological examination of liver and spleen sections with hematoxylin and eosin and Masson trichrome staining with immunohistochemical detection of splenic CD3 and CD20 lymphocytes, S100A9 and β actin antibodies were detected. Morphometric and statistical analyses of the results were performed. TAA administration altered the histological structure of the liver and spleen and impaired liver function. It increased the expression of splenic CD3, CD20 lymphocytes, and S100A9 while diminishing the expression of β actin. Each of rapamycin and filgrastim, when administered separately, improved liver and spleen indices and liver function, but rapamycin did not affect the albumin level. They lowered splenic B and T lymphocyte levels. Expression levels of S100A9 showed down-regulation while β actin levels were up-regulated when compared with TAA. Combination therapy improved liver and spleen tissue pathology and significantly ameliorated the expression of splenic lymphocytes through regulation of S100A9 and β actin expression. The synergistic effect of combination therapy was dependent on the regulation of splenic S100A9 and β actin levels.

Alzheimer's disease (AD) has a significant financial impact on society since it is believed to be the most common neurological condition and one of the main causes of death for the elderly. Curcumin's remarkable pharmacological effects were hampered by its low bioavailability. Applying curcumin in its nanoform, which would enable it to traverse the blood-brain barrier, might help get over these restrictions. This current study aimed to investigate the neuroprotective effects of nanocurcumin on the AD induced by aluminum chloride "AlCl3". 24 Swiss albino rats were divided into four groups; (I) negative control , group (II) diseased, group (III) protective, group (IV) therapeutic. At the end of experiment, behavioral test, assessment of biochemical markers, gene expression of neurogranin (RC3) and β-amyloid protein (APP), expression of phosphorylated Tau (p-Tau) and Glial fibrillary acidic protein (GFAP) imunohistochemically, and histopathological changes in the studied groups. Curcumin nanoform particles decreased the he number of errors and the latency to escape box in the preventive and therapeutic rats. Furthermore, they reduced the oxidative stress induced by AlCl3 in brain tissue, down-regulated the relative expression of RC3 and APP in hippocampus and improve the histopathological alterations in brain tissue. Curcumin coated with chitosan nanoparticles boosted drug permeability across the blood-brain barrier, boosted microglia activation, and accelerated the phagocytosis of the Aβ peptide, suggests that curcumin was among the most intriguing and promising compounds for developing therapies for AD. Additionally, neurogranin (Ng) as a post-synaptic membrane protein can be a promising tool for early diagnosis of cognitive decline.

Background: Wound healing is a complex process necessary for repairing damaged tissues and preventing infection. Selenium nanoparticles (Se NPs) were known by their antioxidant and antimicrobial effects, also niacin has angiogenesis and antioxidant effect that is important in wound healing. Objective: The present study was to investigate the effect of Se NPs and niacin in reducing and accelerating the wound healing time in mice. Methods: A simple wet chemical method has been modified to synthesize Se NPs in order to investigate their effect and niacin on reducing the wound healing in 80 adult female albino mice (250 mm2 full thickness open excision wound) that were divided into eight groups (10 mice/each). After 30-daymice were sacrificed, blood and tissue samples were taken for analysis. Results: The results showed that the percentage of wound area has been significantly reduced in Se NPs and niacin treated groups compared to the positive control. The level of Vascular Endothelial cell Growth Factor and Collagenase I in Se NPs and niacin groups significantly exceed those of other groups while nitric oxide (NO) was significantly decreased in treated groups. Liver and kidney functions showed Se NPs and niacin lower toxicity effect. Skin tissue showed the wound healing effect of Se NPs and niacin by regenerating skin layer compared to the positive group. The high antioxidant property and low hemolysis activity of Se NPs and niacin proved the biocompatible nature of Se NPs and niacin. A possible mechanism depends on the obtained results has been proposed. Conclusion: Se NPs and niacin play an important role in accelerating and reducing the time of wound healing while they were antagonistic to each other.

Background: Chlorpyrifos (CPF) is one of the most widely used Organophosphates (OPs) insecticides in agriculture and public health. Natural products (Propolis and Nigella Sativa) are a promising source for the discovery of new pharmaceuticals. Aim: The present study was an attempt to evaluate the benefits of Propolis and Nigella Sativa alone and in combination against toxicity induced by Chlorpyrifos in on lung and heart tissues of adult male albino rats. Materials & Methods: 54 adult male albino rats were equally divided into 9 groups as following: Group I (negative control group); Group II: received the solvent. Group III (Propolis treated group): in which each rat received orally Propolis only rats (400mg/kg body weight) dissolved in corn oil. Group IV (Nigella Sativa oil treated group) each rat received orally Nigella Sativa oil (100 mg/kg) dissolved in corn oil. Group V: (Propolis and Nigella Sativa treated group). Group VI (CPF treated group): rats gavaged orally CPF at a daily dose of 6.75 mg/kg (1/20 of the oral LD50 of CPF (135mg/kg) dissolved in corn. Group 7 (CPF and Propolis treated group): rats gavaged orally Propolis before CPF administration. Group 8 (CPF and Nigella Sativa oil treated group): the rats gavaged orally Nigella Sativa before CPF. Group 9 (CPF, Nigella Sativa oil and Propolis treated group). Results: Chlorpyrifos induced a highly significant increase in lactate dehydrogenase, creatine kinase activities, elevation of Galctin-3 and troponin levels, and a significant reduction in acetylcholine esterase activity. All these alterations were confirmed histopathologically in lung and heart tissues, where Chlorpyrifos induced myocardial necrosis, muscular hyalinosis, bronchopneumonia and bronchitis. Meanwhile, Propolis and Nigella Sativa showed a protective action against Chlorpyrifos toxic effects especially when used in combination. Conclusion: It can be concluded that Propolis and Nigella Sativa had an ameliorating effect against this toxicity induced in adult albino rats.