8 research outputs found

    Salvia verticillata Improved Cognitive Deficits in a Chronic Cerebral Hypoperfusion Rat Model

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    CCH, resulting from multiple cerebrovascular diseases, has been considered the primary cause of cognitive impairment in recent years. In this process, oxidative stress plays a critical role and damages hippocampal neurons. Research has shown that Salvia verticillata has a significant antioxidant and free radical-scavenging activity due to its polyphenolic compounds. Therefore, the present study aimed to evaluate the effect of Salvia verticillata on a rat model of chronic cerebral hypoperfusion. A total of 24 rats were subjected to Salvia verticillata or vehicle orally from one week before 2VO surgery for 14 days. Cerebral hypoperfusion was induced by the bilateral occlusion of the common carotid arteries (2VO, n = 12 and sham, n = 12). The cognition of rats was evaluated 1 week after surgery in the MWM. In the MWM test, 2VO rats showed longer escape latency time and swimming distance and spent a shorter time in the target quadrant (p 0.05). Our results indicated that Salvia verticillata treatment significantly improved cognitive deficits in cerebral ischemic rats, probably by reducing oxidative stress damage

    Evaluating polyethyleneimine/DNA nanoparticles-mediated damage to cellular organelles using endoplasmic reticulum stress profile

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    Gene therapy has emerged as an influential tool for treating the genetic and specific acquired disorders. Among all kinds of gene delivery systems, the cationic polymer polyethyleneimine (PEI) is considered as a promising non-viral gene delivery vector, although there are still concerns about its magnitude of cytotoxicity. While any cell insult leads to unfolded/misfolded protein accumulation and its consequent unfold protein response, evaluating the expression profile of ER-stress genes would be a sensitive indicator of cell stress. Beside cytotoxicity assays, real-time RT-PCR was used to investigate the effects of PEI nanoparticles on the endoplasmic reticulum. Treating Neuro2A cells revealed that PEI can induce cell toxicity in a concentration-dependent manner. Also, It increased the transcript levels of Grp78 (Bip), Atf4 and Chop, and splicing of Xbp1. To further optimize the transfection properties in Neuro2A cells, PEI was used to deliver a plasmid DNA containing GFP reporter. While different PEI/plasmid ratios revealed similar transfection efficiency, increasing the PEI/plasmid ratio led to induction of ER-stress markers. These results underscored that beside the effectiveness of PEI, using the lowest possible ratio of PEI/plasmid would minimize the detrimental effects of PEI on cells and confer it a beneficial therapeutic importance in nucleic acid delivery

    Histopathological Study of Protective Effects of Honey on Subacute Toxicity of Acrylamide-Induced Tissue Lesions in Rats’ Brain and Liver

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    Background: The therapeutic potential of honey is related to antioxidant activity against reactive oxygen species because it contains compounds such as polyphenols; therefore, we evaluated the potential protective effect of honey on subacute toxicity of ACR by histopathologic study on tissue lesions in rat. Methods: In Ferdowsi University of Mashhad, Mashhad, Iran, 2016, male Wistar rats were divided into 7 groups. To induce toxicity, ACR was injected (50 mg/kg for 11 d) to rats in 5 groups. In treatment groups, rats received three doses of honey 1.25, 2.5, and 5 g/kg in addition to the ACR. The two remaining groups received vitamin E (200 IU/kg) and normal saline as positive and negative control respectively. On the last day, after necropsy, tissue specimens from brain and liver were collected for histopathological studies. Results: Receiving of ACR caused tissue injuries including degeneration, necrosis, hyperemia, hemorrhage and inflammation in liver; ischemic cell change, hyperemia, hemorrhage and edema in brain tissue. Administration of honey considerably reduced tissue damages caused by ACR, particularly with dosage 5 g/kg. Conclusion: The severity of tissue lesions caused by the ACR can be reduced by honey, likely through its antioxidant activity. Increasing concentrations of honey will enhance its effectiveness
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