Lithium decreases streptozocin-induced diabetic neuropathy in rats by inhibiting of adenosine triphosphate (ATP) degradation

One of the most frequent complications of diabetes is diabetic peripheral neuropathy. Hyperglycemia would result in the advancement of this condition over a period of time. The most effective way in preventing diabetic neuropathy is regular control of glucose. In this study; we evaluated the effects of lithium onstreptozocin (STZ)-induced diabetic neuropathy in rats. Diabetic neuropathy was created 7 weeks after administration of STZ (45 mg/kg). Lithium was added to drinking water (450 mg/l) for 7 weeks and its plasma level after this period of time was 0.17±0.02 mmol/l. Levels of adenosine triphosphate (ATP) in dorsal root ganglion (DRG) neurons, oxidative stress parameters, open-field activity test and morphological analysis were assessed in this investigation. Currentresults showed significant elevation of oxidative stress biomarkers, reduction of ATP, abnormal morphology of DRG neurons and decrease of total distance moved in rats with STZ-induced diabetic neuropathy. The alterations in mentioned parameters were considerably restored by lithium treatment. These findings provide evidence for protective effects of lithium on STZ-induced diabetic neuropathy. © 2018 Tehran University of Medical Sciences. All rights reserved

Lithium decreases streptozocin-induced diabetic neuropathy in rats by inhibiting of adenosine triphosphate (ATP) degradation

One of the most frequent complications of diabetes is diabetic peripheral neuropathy. Hyperglycemia would result in the advancement of this condition over a period of time. The most effective way in preventing diabetic neuropathy is regular control of glucose. In this study; we evaluated the effects of lithium onstreptozocin (STZ)-induced diabetic neuropathy in rats. Diabetic neuropathy was created 7 weeks after administration of STZ (45 mg/kg). Lithium was added to drinking water (450 mg/l) for 7 weeks and its plasma level after this period of time was 0.17±0.02 mmol/l. Levels of adenosine triphosphate (ATP) in dorsal root ganglion (DRG) neurons, oxidative stress parameters, open-field activity test and morphological analysis were assessed in this investigation. Currentresults showed significant elevation of oxidative stress biomarkers, reduction of ATP, abnormal morphology of DRG neurons and decrease of total distance moved in rats with STZ-induced diabetic neuropathy. The alterations in mentioned parameters were considerably restored by lithium treatment. These findings provide evidence for protective effects of lithium on STZ-induced diabetic neuropathy. © 2018 Tehran University of Medical Sciences. All rights reserved

Silymarin-albumin nanoplex: preparation and its potential application as an antioxidant in nervous system in vitro and in vivo

In this study, we formulated silymarin-HSA nanoplex and assayed its ability to reduce LPSinduced toxicity in vitro and in vivo. Silymarin molecules were encapsulated into HSA nanoplex and the loading efficiency and characterization of fabricated nanoplex were performed by using HPLC, TEM, SEM, DLS, FTIR analysis, and theoretical studies. Afterwards, their protective effect against LPS (20 µg/ml) -induced toxicity in SH-SY5Y cells was investigated by MTT, ROS, and apoptosis assays. For in vivo experiments, rats were pre-treated with either silymarin or silymarin -HSA nanoplex (200 mg/kg) orally for 3 days and at third day received LPS by IP at a dose of 0.5 mg/kg, 150 min before scarification followed by SOD and CAT activity assay. The formulation of silymarin-HSA nanoplex showed a spherical shape with an average diameter between 50 nm to 150 nm, hydrodynamic radius of 188.3 nm, zeta potential of -26.6 mV, and a drug loading of 97.3%. In LPS-treated cells, pretreatments with silymarin-HSA noncomplex recovered the cell viability and decreased the ROS level and corresponding apoptosis more significantly than free silymarin. In rats, it was also depicted that, silymarin-HSA noncomplex can increase the SOD and CAT activity in brain tissue at LPS-triggered oxidative stress model more significantly than free counterpart. Nanoformulation of silymarin improved its capability to reduce LPS-induced oxidative stress by restoring cell viability and elevation of SOD and CAT activity in vitro and in vivo, respectively. Therefore, formulation of silymarin may hold a great promise in the field of antioxidant agent development

Ethyl acetate and methanolic extracts from three algae and their potential antioxidant activity in vitro

Marine algae produce secondary metabolites with antioxidant activity and therapeutic effects. The aim of this study was to evaluate the antioxidant activity of ethyl acetate and methanolic extracts of three algal species: Nannochloropsis oculata (Droop) D.J. Hibberd, Enteromorpha sp., and Polysiphonia scopulorum Harvey. Ethyl acetate and methanolic extracts were prepared using the percolation method and evaluated for DPPH radical scavenging activity, nitric oxide scavenging activity, metal chelating activity, and reducing power activity. The means were compared using the Newman-Keuls Multiple Comparison test. The ethyl acetate extract of N. oculata was found to have the highest total phenol content (82.07 ± 1 .32 mg gallic acid equivalent g-1 of extract). The maximum flavonoid content belonged to Enteromorpha sp. (74.79 ± 0.91 quercetin equivalent g-1 of extract). The maximum DPPH radical scavenging activity (67.73 ± 0.39) belonged to ethyl acetate extract of P. scopulorum. The maximum nitric oxide scavenging activity and metal chelating activity belonged to ethyl acetate extract of N. oculata. The highest reducing power activity was observed in the methanolic extract of P. scopulorum. Ethyl acetate extracts of P. scopulorum and N. oculata show significant antioxidant activity, which may be due to their phenolic and flavonoid compounds. © Begell House Inc., 2019

Tropisetron attenuates amyloid-beta-induced inflammatory and apoptotic responses in rats

Background Alzheimer's disease (AD) is a neurodegenerative disorder featured by deposition of beta-amyloid (Ab) plaques in the hippocampus and associated cortices and progressive cognitive decline. Tropisetron, a selective 5-HT3 receptor antagonist, is conventionally used to counteract chemotherapy-induced emesis. Recent investigations describe antiphlogistic properties for tropisetron. It has been shown that tropisetron protects against rat embolic stroke. We investigated protective properties of tropisetron in a beta-amyloid (Ab) rat model of AD and possible involvement of 5-HT3 receptors. Material and methods Aβ (1-42) was injected into the hippocampus of male rats. Animals were treated intracerebroventricularly with tropisetron, mCPBG (selective 5-HT3 receptor agonist) or mCPBG plus tropisetron on days 1, 3, 5 and 7. Seven days following Ab administration, inflammatory markers (TNF-α, COX-2, iNOS and NF-κB), apoptotic markers (caspase 3 cytochrome c release) and calcineurin phosphatase activity were assessed in hippocampus. Results Seven days following Ab inoculation, control animals displayed dramatic increase in TNF-α, COX-2, iNOS, NF-κB, active caspase 3, cytochrome c release and calcineurin phosphatase activity in the hippocampus. Tropisetron significantly diminished the elevated levels of these markers and reversed the cognitive deficit. Interestingly, tropisetron was also found to be a potent inhibitor of calcineurin phosphatase activity. The selective 5-HT3 receptor agonist mCPBG, when co-administered with tropisetron, completely reversed the procognitive and anti-apoptotic properties of tropisetron while it could only partially counteract the anti-inflammatory effects. mCPBG alone significantly aggravated Ab-induced injury. Conclusion Our findings indicate that tropisetron protects against Aβ-induced neurotoxicity in vivo through both 5-HT3 receptor-dependent and independent pathways. copy; 2013 Stichting European Society for Clinical Investigation Journal Foundation