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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]

Lawsone, a naphthoquinone phytochemical compound present in the plants such as henna, was found to increase the healing process. However, clinical applications are impeded owing to the poor water solubility, low bioavailability, and dyeing property to the hair and skin. Nanostructured lipid carriers (NLCs) are appropriate carriers that cover undesirable effects of drugs, afford sustained release over a prolonged period of time, reduce systematic effects, decrease irritation, and increase tolerance. In this research, a formulation of lawsone incorporated NLC was prepared, and characterized for pharmaceutical application. The synthesized formulation was characterized using electron microscopy, polydispersity index, and zeta potential, and entrapment efficiency and malondialdehyde (MDA) level were evaluated. In order to assess wound healing potential, the wound area was measured at different times post-treatment, showing a structured tissue with better healing signs in NLC- Lw- Lv group in comparison with alpha ointment. NLC- Lw- Lv (NLC containing lawsone and lavender) formulation with mean size of 165.3 ± 4.2 nm, polydispersity index of 0.211, zeta potential of − 24.3 mV, and entrapment efficiency of 79.3 ± 2.9 was subjected to further experiments as optimized formulation. The ex vivo evaluation of formulation in mouse skin indicated better retention, less residue, and permeation in comparison with alpha ointment as standard. MDA level, as the indicator of lipid peroxidation, was lower in the NLC- Lw- Lv treated group. Histological score of microscopic wound healing parameters, such as swelling, re-epithelialization, formation of fibrotic tissue, and granulation, presented significantly better wound contraction in NLC- Lw- Lv treated group. In conclusion, our results propose the effective wound healing ability of lawsone, proved by more effective and an earlier stimulation of wound contraction. [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]

The binuclear iron(III) complex (1), namely, {[Fe(5,5′-dmbpy)2(OH2)]2(µ-O)}(NO3)4 with a distorted octahedral coordination, formed by four nitrogen and two oxygen atoms, was previously reported by our team. In this study the DNA-binding and cytotoxicity evaluation for target complex were studied. The results indicated strong cytotoxicity activity against A549 cells comparable to cisplatin values. The binding interaction between complex 1 and FS-DNA was investigated by UV–Vis, fluorescence spectroscopy, and gel electrophoresis at physiological pH (7.2). The DNA binding investigation has shown groove binding interactions with complex 1, therefore the hydrogen binding plays an important role in the interaction of DNA with complex 1. The calculated thermodynamic parameters (ΔH°, ΔS° and ΔG°) show that hydrogen bonding and Vander–Waals forces have an important function in Fe(III) complex–DNA interaction. Moreover, DNA cleavage was studied using agarose gel electrophoresis. Viscosity measurements illustrated that relative viscosity of DNA was unchanged with the adding concentrations of Fe(III) complex. Molecular docking simulation results confirmed the spectroscopic and viscosity titration outcomes. [ABSTRACT FROM AUTHOR]

In the following, the cellular and molecular mechanism of cytotoxicity induced by prodrug dacarbazine toward the isolated rat hepatocytes was studied. Accelerated cytotoxicity screening technique (ACMS) was used to perform this study. Addition of dacarbazine to isolated rat hepatocytes resulted in reactive oxygen species (ROS) formation, and lysosomal membrane leakiness before hepatocyte lysis occurred. Hepatocyte ROS generation was inhibited by desferoxamine (a ferric chelator). Cytotoxicity was prevented by antioxidants or ROS scavengers (mannitol or dimethylsulfoxide), cytochorome P450 inhibitors (phenylimidazole, diphenyliodonium chloride, 4-methylpyrazole, and benzylimidazole). In addition to lysosomal damage, dacarbazine caused hepatocyte protease activation and cell proteolysis. Dacarbazine cytotoxicity is associated with ROS (H2O2, O) generation. It is suggested that H2O2 could cross the lysosomal membrane, react with lysosomal Fe2+ to form hydroxyl radical (Haber-Weiss reaction) which is the major cause of lysosomal membrane leakiness, proteases, and other digestive enzymes' release and finally the cell death. [ABSTRACT FROM AUTHOR]

In this study, the interaction between (2,2ʹ-bipyridine)(pyrrolidinedithiocarbamato) platinum(II) nitrate, [Pt(bpy)(pyr-dtc]NO, and human serum albumin (HSA) was investigated by various spectroscopic methods (UV-vis, fluorescence, CD and FT-IR) and molecular docking technique at three temperatures. UV-vis absorption spectroscopy showed that Pt(II) complex can denature the protein at moderate concentrations. The results of emission quenching at two temperatures has revealed that the quenching mechanism of Pt(II) complex with HSA was static quenching mechanism. Binding constants ( K), binding site number ( n) and corresponding thermodynamic parameters ∆ G˚, ∆ H˚ and ∆ S˚ were calculated and revealed that hydrophobic forces played a major role when Pt(II) complex interacted with HSA. The binding distance ( r) between above complex and HSA based on Försterʼs theory of non-radiation energy transfer was calculated as 3.22 nm. Alterations of HSA secondary structure induced by complex were confirmed by FT-IR and CD measurements. Also, a molecular docking study was performed for identification of key structural features of binding of the Pt complex into the receptor and predicting bioactive conformers. Our results may provide valuable information to understand the mechanistic pathway of drug delivery and to pharmacological behavior of drug. [ABSTRACT FROM AUTHOR]