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Background and Objective: Cervical cancer is the fourth most common cancer in the world. The most important issue in cancer treatment is the destruction of cancer cells in the presence of normal cells. For this reason, it is necessary to use natural resources such as plants to treat cancer. The aim of this study is to evaluate the antibacterial effects of the ethanolic extract of Alhagi maurorum on Staphylococcus aureus and Pseudomonas aeruginosa and cytotoxicity on HeLa cervical cancer cell line. Methods: In this experimental study, first the ethanolic extract of Alhagi maurorum was prepared, and then the two standard strains of Staphylococcus aureus (ATCC: 25923) and Pseudomonas aeruginosa (ATCC: 27853) were lyophilized by culturing in nutrient medium. In order to confirm the standard strains, biochemical tests were performed. Microdilution method was used to determine the minimum inhibitory concentration and after obtaining the minimum inhibitory concentration, the minimum bactericidal concentration was evaluated. Furthermore, the effects of the cytotoxicity of the extract at concentrations of 0.1, 10, 50, 100, 500 and 1000 μg/ml was evaluated on the HeLa cell line in a period of 48 hours using the MTT method and comparing its toxicity with the cisplatin group (positive control group). Findings: Ethanol extract of Alhagi maurorum at a concentration of 50 μg/ml reduced the growth of cancer cells, and in the statistical comparison, 50, 500 and 1000 μg concentrations revealed significant differences (p<0.05). According to minimum inhibitory concentration results, the minimum growth inhibitory concentration of the extract on the standard strain of Staphylococcus aureus and Pseudomonas aeruginosa was reported to be 4000 and 16000 μg/ml, respectively, and according to minimum bactericidal concentration results, the minimum bactericidal concentration of the extract was found 4 times the minimum inhibitory concentration (16000 μg/ml) in Staphylococcus aureus (ATCC: 25923), but it was not lethal in Pseudomonas aeruginosa (ATCC: 27853). Conclusion: The results of the study showed that the ethanolic extract of Alhagi maurorum affected HeLa cells through antioxidant activity and inhibited their growth, and according to minimum inhibitory concentration and minimum bactericidal concentration results, it was also shown that the most inhibitory effect was on the standard strain of Staphylococcus aureus while it showed no effects on the strain of Pseudomonas aeruginosa. [ABSTRACT FROM AUTHOR]

Introduction: Considering the numerous drug resistance in cancer and the advancement of science in nanomedicines, it was decided to compare the effectiveness of zinc oxide nanoparticles in colon and prostate cell lines. Considering the importance of factors and Oxidative stress pathways in cancer prevention, the aim of the study is based on oxidative stress mechanisms., Methodes: In order to evaluate the effects of zinc oxide nanoparticles on colon and prostate cell lines, oxidative stress factors ROS, MDA, and GSH and mitochondrial function were evaluated. The data was analyzed with Prism v8 software, and the significance level was considered to be P  < 0.05., Results: The results showed that nanoparticles induce ROS and reduce intracellular glutathione by destroying and disrupting mitochondrial function, and by increasing ROS production, damage to the lipid membrane and an increase in MDA were also evident. This effect was dose-dependent and the greatest at a concentration of 25 μg/mL. Also, ZnO nanoparticles performed better in the HT29 cell line than in the PC3 cell line., Conclusion: This study showed that exposure of HT29 and PC3 cancer cells to zinc oxide nanoparticles at different concentrations inhibited growth by cytotoxic effects., Competing Interests: All authors declare that they have no conflict of interest., (© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Oxidative stress plays a prominent role in expanding toxicity and various diseases. This study investigated the potential protective effects of ginger ( Zingiber officinale ) rhizome extract and NAC on docetaxel induced genotoxicity and oxidative stress. The antioxidant power of NAC and ginger extract on the genetic toxicity induced by docetaxel was assessed by micronucleus test. The ROS test with DCFH reagent was used to assess the reactive oxygen species. The thiobarbituric acid method was used to evaluate the amount of MDA produced by docetaxel. The amounts of phenol and flavonoids in the ginger extracts were also evaluated. The amount of phenol in the ginger extract was 0.886 mg of gallic acid per gram of dry extract. The amount of flavonoids were 0.242 mg/mL of quercetin per gram of dry extract. As shown by the micronucleus results, concentrations of 100 and 500 μM NAC and all concentrations of the ginger extract significantly reduced the number of micronuclei produced by docetaxel. On the other hand, the results of oxidative stress tests (ROS and LPO) showed that docetaxel in HGF cells increased the production of ROS and LPO, and the concentrations of ginger extract and NAC decreased oxidative stress in HGF cells in a dose-dependent manner. The results indicate that using these two antioxidants helps inhibit genetic toxicity and oxidative stress caused by docetaxel.

Metformin exerts its anticancer effect through two mechanisms, directly affecting the tumor and indirectly reducing systemic insulin levels. The anticancer effects of aspirin occur by inhibiting Cyclooxygenase (COX)-2. COX-2 is absent in many cell types under normal conditions and increases under pathological conditions such as cancer. This study aims to investigate the effect of metformin and aspirin and their combination of them on A549 and PC3 cell lines. Metformin and aspirin were investigated separately and in combination on two cancer cell lines, A549 and PC3. The examined groups include the negative control of untreated cells and the positive control of cisplatin and drugs at concentrations of 15, 10, and 20 μg/ mL to investigate the mechanism of oxidative stress factors (reactive oxygen species, lipid peroxidation, Glutathione (GSH)) and apoptosis (lactate dehydrogenase). The results showed that aspirin, metformin, and their combination could affect cancer cell growth by damaging mitochondria, releasing reactive oxygen species, and activating the oxidative stress pathway. Also, these two drugs show the activation of the apoptotic pathway in cancer cells by increasing the lactate dehydrogenase factor and releasing it from the cells. By disrupting the balance of oxidants and antioxidants in the cell, metformin and aspirin cause an increase in the level of reactive oxygen species and a decrease in the level of glutathione reserves, followed by an increase in the level of lipid peroxidation and a decrease in cell viability. Unlike common chemotherapy drugs, these drugs have no known severe side effects; Therefore, in the not-so-distant future, these drugs can also be used as anticancer drugs., Highlights: Metformin and aspirin, commonly used drugs for diabetes and inflammation, inhibit the growth of cancer cell lines, A549 and PC3.Metformin and aspirin, either separately or in combination, can potentially impede cancer cell growth by disrupting mitochondrial function, inducing the release of reactive oxygen species (ROS), and activating oxidative stress pathways.Furthermore, these drugs can trigger apoptosis, a programmed cell death mechanism, in cancer cells by increasing lactate dehydrogenase (LDH) levels and facilitating its release from the cells., Competing Interests: None declared., (© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Introduction: Paroxetine is functionally classified as a selective serotonin reuptake inhibitor. Paroxetine can induce mitochondria-dependent apoptosis through the ROS-MAPK pathway.Amitriptyline is a tricyclic antidepressant. This drug induces the expression of p53, thereby activating caspase-3. Amitriptyline has also been studied as a potential candidate for inducing oxidative stress and cytotoxicity in cancer cells, which may be more effective than other chemotherapy drugs. This study aims to to investigate the anticancer effects of paroxetine and amitriptyline and their combination treatment on HT29 and A549 cell lines for the first time., Methods: In order to investigate the anticancer effect of two drugs, paroxetine and amitriptyline, on inhibiting the growth of A549 and HT29 cancer cells, oxidative stress factors and LDH enzyme and apoptosis tests were performed., Results: Two drugs, amitriptyline and paroxetine alone, inhibited the growth of cancer cells in such a way that the inhibitory effect of the cells increased with the increase in the dose of the drug. In the simultaneous exposure of these two drugs, the inhibitory effect was much greater than the effect of single drug exposure. Also, these two drugs have caused LDH leakage and induction of apoptosis., Conclusion: According to the results of the study, it was found that these two drugs have the necessary ability to inhibit the growth of cancer cells by inducing apoptosis and LDH leakage and inducing oxidative stress., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

The linkage between inflammation and oxidative stress in liver damage has been proven and is undeniable; dexamethasone with some antioxidants can reduce the toxicity of liver tissue. Due to the importance of cancer treatment, glucocorticoids' synergistic effect in inhibiting cancer cell growth is also investigated. Dexamethasone alone and combined with etoposide were tested at concentrations of 1, 5, and 10 μM to evaluate the potency of dexamethasone in inhibiting the growth of A549 cells using oxidative stress factors and DNA damage. Also, intraperitoneal injection of dexamethasone in rats was used to induce liver toxicity. Coenzyme Q10 at different concentrations (1, 10, and 50 mg/kg) was used as an antioxidant to assess the oxidative stress factors and measure Caspase-3 activity. The results showed that dexamethasone combined with etoposide could significantly inhibit the growth of cancer cells and induce apoptosis. Treatment of A549 cells using dexamethasone also inhibits cancer cells' growth by inducing oxidative stress and DNA damage. Dexamethasone also, by inducing oxidative stress and activation of caspase 3, ultimately causes hepatotoxicity. Treatment with different concentrations of CoQ10 showed improved mitochondrial function, antioxidant defense, and liver enzyme. The best effect of coenzyme Q10 on dexamethasone-induced hepatotoxicity is 50 mg/kg. As a result, dexamethasone (alone and combined with etoposide) has an anti-cancer effect by damaging DNA and inducing oxidative stress. Also, CoQ10 has antioxidant effects against dexamethasone-induced hepatotoxicity by improving mitochondrial function and reducing caspase-3 activity.

Objectives: Nanotechnology has helped a lot in diagnosing and treating multiple illnesses, specifically cancer, and increasing the development of targeted drug delivery methods. Nanocomposites are materials with at least one component smaller than 100 nm. Therefore, this study aims to assess the anticancer effects of silver-graphene nanocomposite on MCF-7., Materials and Methods: In this study, the rate of inhibition of cancer cell growth and production of reactive oxygen radicals, malondialdehyde, and glutathione stores in MCF7 cells were investigated. Cancer cells were exposed to nano particles for 48 hr. Silver nanoparticles and graphene both reduced the growth rate of MCF-7., Results: Subsequently, by treating the cells with silver-graphene nanocomposite, the rate of inhibition of cell growth at the highest concentration was 84.60%. Nanoparticles also inhibited the growth of cancer cells through the oxidative stress pathway by increasing the amount of intracellular ROS, followed by increasing malondialdehyde and decreasing glutathione stores, so that at the highest combined concentration of nanoparticles, the amounts of LPO and ROS increased up to 70% and 74 %, and glutathione reserves decreased by 16%., Conclusion: Treatment of MCF-7 cells with silver or graphene nanoparticles and combination treatment with these two substances against cisplatin have sound effects, and by affecting oxidative stress factors, such as increased ROS and subsequent increase in lipid membrane damage, inhibit cell growth and proliferation. According to the mathematical model, silver graphene nanocomposite> silver nanoparticles> graphene has the best effect in inhibiting the growth of cancer cells, respectively., Competing Interests: All authors declare that they have no conflicts of interest.

Depression is a very common mental disorder and mechanism that is associated with mitochondrial dysfunction. In the present study, we examined the mechanisms of action of isolated brain mitochondria in rats with depression for the first time. This will help identify the mitochondrial protective pathways of the two drugs and shed light on new therapeutic goals for developing antidepressants. Forced swimming, tail suspension, and sucrose preference tests were used to assess depressive-like behaviors and the oxidative stress factors of brain tissue, and measure the gene expression of apoptotic and anti-apoptotic, neuroplasticity, and neuroinflammatory factors by RT-PCR and acetylcholinesterase (AChE) activity in brain tissue (hippocampus and prefrontal) and the serum levels of corticosterone and fasting blood sugar. The results showed that the separation of neonatal rats from their mothers induced depressive-like behaviors, weight loss, mitochondrial dysfunction, increased expression of genes involved in neuroinflammation, apoptosis, genes involved in the depressive process, and decreased expression of genes involved in mood in both the hippocampus and prefrontal cortex. Maternal separation increased serum corticosterone levels, caused dysfunction of the cholinergic system, and also increased AChE activity. Treatment with different concentrations of minocycline and edaravone (1, 20, and 50 mg/kg), 5MTHF, and citalopram for 14 days showed that these drugs improved depression-like behaviors and mitochondrial function. It also reduced the expression of genes involved in neuroinflammation, apoptosis, and depression and increased the expression of genes involved in mood. In conclusion, minocycline and edaravone have neuroprotective, mitochondrial protective, antioxidant, anti-inflammatory, and anti-apoptotic effects against depressive-like behaviors caused by chronic stress., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Introduction: Clostridium perfringens is a type of gram-positive anaerobic bacilli. C.perfringens produces many toxins, of which epsilon (ε) is one of the major ones. The mechanism of epsilon's toxicity is located in the lipid of cell membrane tissues. Epsilon toxin is known as a bioterrorism agent. Inhalation of these aerosols can destroy pulmonary vascular endothelial cells and cause lung injury, which increases vascular permeability and pulmonary edema., Methods: In this study, we investigated the toxicity of epsilon toxin by using the MTT assay, evaluated oxidative stress effects such as ROS and LPO using the DCFH and TBA reagents, and measured the GSH of the normal and lung cancer cells by using the DTNB reagent., Results: The result showed that 1 μg/ml of epsilon toxin caused mitochondrial disorder and reduced the growth of the normal cell line. This toxin also induced ROS and damage to lipid membranes. Furthermore, the same effect occurred in the lung cancer cell, and the epsilon toxin inhibited cancer cell proliferation., Conclusion: This toxin causes toxicity by binding to lipid membranes. As the present study results have confirmed, epsilon toxin inhibits mitochondrial function and induces ROS and lipid membrane damage., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

In continuation of our research to find strong and safe anticonvulsant agents, a number of (arylalkyl)azoles (AAAs) containing naphthylthiazole and naphthyloxazole scaffolds were designed and synthesized. The in vivo anticonvulsant evaluations in BALB/c mice revealed that some of them had significant anticonvulsant activity in both maximal electroshock (MES) and pentylenetetrazole (PTZ) models of epilepsy. The best profile of activity was observed with compounds containing imidazole and triazole rings (C1, C6, G1, and G6). In particular, imidazolylmethyl-thiazole C1 with median effective dose (ED 50 )= 7.9 mg/kg in the MES test, ED 50 = 27.9 mg/kg in PTZ test, and without any sign of neurotoxicity (in the rotarod test, 100 mg/kg) was the most promising compound. The patch-clamp recording was performed to study the mechanism of action of the representative compound C1 on hippocampal dentate gyrus (DG) cells. The results did not confirm any modulatory effect of C1 on the voltage-gated ion channels (VGICs) or GABA A agonism, but suggested a significant reduction of excitatory postsynaptic currents (EPSCs) frequency on hippocampal DG neurons. Sub-acute toxicity studies revealed that administration of the most active compounds (C1, C6, G1, and G6) at 100 mg/kg bw/day for two weeks did not result in any mortality or significant toxicity as evaluated by assessment of biochemical markers such as lipid peroxidation, intracellular glutathione, total antioxidant capacity, histopathological changes, and mitochondrial functions. Other pharmacological aspects of compounds including mechanistic and ADME properties were investigated computationally and/or experimentally. Molecular docking on the NMDA and AMPA targets suggested that the introduction of the heterocyclic ring in the middle of AAAs significantly affects the affinity of the compounds. The obtained results totally demonstrated that the prototype compound C1 can be considered as a new lead for the development of anticonvulsant agents., (Copyright © 2021 Elsevier B.V. All rights reserved.)