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Carbon monoxide (CO) is produced via incomplete combustion of fossil fuels and it may cause long-term neurological sequel upon exposure. Hesperidin (HES), a flavanone glycoside found in citrus plants, exerts diverse beneficial health effects. The present study mechanistically examined the neuroprotective effects of HES in CO-poisoned rats. Thirty male Wistar rats (five groups of six animals) were exposed to 3000 ppm CO for 1 h. Immediately after the exposure and on the next 4 consecutive days (totally five doses), rats intraperitoneally received either normal saline (the control group) or different doses of HES (25, 50, and 100 mg/kg). A sham group that was not exposed to CO was also considered. After evaluation of spatial learning and memory using a Morris water maze (MWM), animals were sacrificed and oxidative stress status in blood samples, and Akt, Bax, Bcl2, and brain-derived neurotrophic factor (BDNF) expression in brain samples were assessed. Western blot analysis indicated increased Akt but decreased Bax/Bcl2 levels in the HES 100 mg/kg, and induced BDNF levels in all HES-treated groups. MWM results showed that HES significantly decreased memory loss. The current findings indicate that HES could alleviate neurological impairments induced by CO in rats. [ABSTRACT FROM AUTHOR]

This document is a correction notice for an article titled "Hesperidin neuroprotective effects against carbon monoxide-induced toxicity in male rats" published in Naunyn-Schmiedeberg's Archives of Pharmacology. The correction states that the author name "Zahra Dadrezaei" was mistakenly used and should be corrected to "Seyedehzahra Dadrezaei." The original article has been corrected accordingly. The publisher, Springer Nature, remains neutral regarding jurisdictional claims and institutional affiliations. The authors of the article are Jafar Shahraki, Kaveh Tabrizian, Ramin Rezaee, Behnam Tashakori, Seyedehzahra Dadrezaei, Vahideh Ghorani, Gholamreza Bagheri, Hosseinali Jahantigh, and Mahmoud Hashemzaei. [Extracted from the article]

Supramolecular carriers as a targeted drug delivery system have a significant role in managing the pharmacokinetics and pharmacodynamics of drugs. Therefore, in this project, we used cyclodextrin (CD) as a host molecule for tamoxifen (TMX) and methotrexate (MTX) to evaluate apoptosis mechanism and statistical patterns of release. The flow cytometry analysis showed that combination therapy by anticancer drugs was successful in apoptosis induction compared to free TMX and MTX. Also, real-time PCR and western blot analyses were performed to measure gene expression of Bak1, Bclx, and caspase-3 in estrogen and folate receptor-positive MCF-7 cell lines. All results confirmed that MNPs containing TMX and MTX can significantly increase Bak1/Bclx ratios plus the activity of caspase-3, while free MTX and free TMX showed no effects on triggering apoptosis after 24 h of exposure. According to results of pharmacokinetic studies onto TMX and MTX release, it is revealed that both models that consist of Sahlin-Peppas and Ritger-Peppas create the good fitting curves more than other statistical patterns at both low and high temperatures (37°C and 42°C). For this reason, activation parameters (ΔH‡, ΔS‡, and ΔG‡) were calculated to estimate the favorable model. The lower energy barrier indicates that the Sahlin-Peppas is the favorable model with both diffusion and relaxation process. Therefore, combination therapy by two anticancer drugs, TMX and MTX, utilizing cyclodextrin-based host–guest supramolecular magnetic nanoparticles (CD-MNPs) provided new results for induction of apoptosis and pharmacokinetic model. [ABSTRACT FROM AUTHOR]

Objectives: Liver is the most important and functional organ in the body to metabolize and detoxify endogenous compounds and xenobiotics. The major goal of the present narrative review is to assess the hepatoprotective properties of hesperidin against a variety of natural and chemical hepatotoxins via different mechanisms. Evidence acquisition: Scientific databases such as Scopus, Medline, Web of Science and Google scholar were thoroughly searched, based on different keywords. Results: A variety of natural hepatotoxins such as lipopolysaccharide, concanavalin A and microcystins, and chemical hepatotoxins such as ethanol, acrylamide and carbon tetrachloride have been shown to damage hepatocytes as well as other liver cells. In addition to hepatocytes, ethanol can also damage liver hepatic stellate cells, Kupffer cells and sinusoidal endothelial cells. In this regard, the flavanone hesperidin, occur in the rind of citrus fruits, had been demonstrated to possess widespread pharmacological properties. Hesperidin exerts its hepatoprotective properties via different mechanisms including elevation in the activities of nuclear factor-like 2/antioxidant response element and heme oxygenase 1 as well as the levels of enzymatic and non-enzymatic antioxidants. Furthermore, reduction in the levels of high-mobility group box 1 protein, inhibitor of kappa B protein-alpha, matrix metalloproteinase-9 and C-reactive protein are some other important hesperidin-derived hepatoprotective mechanisms. Conclusion: Based on several research papers, it could be concluded that hesperidin is able to protect against liver damage from inflammation and/or oxidative stress-mediated natural and chemical toxins. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO) produced by incomplete combustion of hydrocarbons, has many toxic effects on different organs, especially the heart and brain that have greater demands for oxygen. The present study aimed to evaluate the protective effects of granulocyte colony stimulating factor (G-CSF) on apoptosis after CO poisoning in rats. Male Wistar rats were exposed to CO 1500 or 3000 ppm for 60 min. Single and multiple doses of G-CSF (10, 50, and 100 μg/kg) were administered to animals. After CO poisoning, carboxyhemoglobin concentration was measured, apoptotic cells were evaluated by TUNEL assay and caspase 3 activity was determined by immunofluorescence. Blood levels of carboxyhemoglobin significantly increased following exposure to both 1500 and 3000 ppm concentrations of CO. However, carboxyhemoglobin levels were significantly higher following exposure to CO 3000 ppm compared to CO 1500 ppm (p < 0.05). Differences in caspase 3 activity between G-CSF and control groups were significant and G-CSF could decrease apoptosis following CO 3000 ppm poisoning (p < 0.001). TUNEL assay showed that in rats treat with 5 doses of G-CSF 100 μg/kg, apoptosis was significantly ameliorated compared to control rats and sham (rats that were not exposed to CO) group (p < 0.05). Concerning caspase 3 activity and apoptosis rate, the best results were found in rats exposed to 3000 ppm and treated with G-CSF 100 μg/kg. In this study, we confirmed that CO poisoning leads to cardiomyocytes apoptosis which could be significantly reduced by G-CSF treatment. [ABSTRACT FROM AUTHOR]

It is very important to investigate the neurotoxic effects of metals on learning and memory processes. In this study, we tried to investigate the effects and time course properties of oral administration of zinc chloride (25, 50, and 75 mg/kg, for 2 weeks), lead acetate (250, 750, 1,500, and 2,500 ppm for 4, 6 and 8 weeks), and their possible mechanisms on a model of memory function. For this matter, we examined the intra-peritoneal injections of nicotine (0.25, 0.5, 1, and 1.5 mg/kg) and bucladesine (50, 100, 300, and 600 nM/mouse) for 4 days alone and in combination with mentioned metals in the step-through passive avoidance task. Control animals received saline, drinking water, saline, and DMSO (dimethyl sulfoxide)/deionized water (1:9), respectively. At the end of each part of studies, animals were trained for 1 day in step-through task. The avoidance memory retention alterations were evaluated 24 and 48 h later in singular and combinational studies. Zinc chloride (75 mg/kg) oral gavage for 2 weeks decreased latency times compared to control animals. Also, lead acetate (750 ppm oral administrations for 8 weeks) caused significant lead blood levels and induced avoidance memory retention impairments. Four-days intra-peritoneal injection of nicotine (1 mg/kg) increased latency time compared to control animals. Finally, findings of this research showed that treatment with intra-peritoneal injections of nicotine (1 mg/kg) and/or bucladesine (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments. Taken together, these results showed the probable role of cholinergic system and protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations. [ABSTRACT FROM AUTHOR]

Dengue virus is an important arbovirus infection which transmitted by the Aedes female mosquitoes. The attempt to control and early detection of this infection is a global public health issue at present. Because of the clinical importance of its detection, the main focus of this review is on all of the methods that can offer the new diagnosis strategies. The advantages and disadvantages of reported methods have been discussed comprehensively from different aspects like biomarkers type, sensitivity, accuracy, rate of detection, possibility of commercialization, availability, limit of detection, linear range, simplicity, mechanism of detection, and ability of usage for clinical applications. The optical, electrochemical, microfluidic, enzyme linked immunosorbent assay (ELISA), and smartphone-based biosensors are the main approaches which developed for detection of different biomarkers and serotypes of Dengue virus. Future efforts in miniaturization of these methods open the horizons for development of commercial biosensors for early-diagnosis of Dengue virus infection. [ABSTRACT FROM AUTHOR]