AlCl3 Group Research Articles

The Protective Effect of Berberine Against Memory Impairment Induced by Intrahippocampal Injection of Aluminium Chloride in Rats

Background and Objectives: Aluminum is a component of environmental pollutants, which causes neurotoxicity. Berberine is in the group of plant-derived alkaloids such as barberry and its beneficial therapeutic properties in various diseases have been proven. The aim of the present study was to investigate the protective effect of berberine on aluminum-induced neurotoxicity. Methods: In this experimental study, 32 male Wistar rats were randomly divided into 4 groups: sham, berberine-receiving sham, lesions-seeing and berberine-receiving lesions. To induce neurotoxicity, a solution of aluminum chloride (AlCl3) dissolved in distilled water was injected at 5 µL at a dose of 0.37 mg/kg to the left of the dorsal hippocampus. The treated rats received 100 mg/kg of berberine daily from one hour before surgery to one week after surgery and orally. In the fourth week, all groups were tested for behavioral learning and memory using the shuttle box. At the end, malondialdehyde, protein, ROS levels and acetylcholinesterase activity were measured. The results were analyzed using one-way ANOVA test and Tukey test. Results: In the treated AlCl3 group compared to the AlCl3 group, the initial delay was not significantly different but the delay during transit was significantly increased. MDA and ROS levels and acetylcholinesterase activity showed a significant decrease. Conclusion: The results of this study showed that although treatment with berberine in the lesion group by aluminum chloride did not cause a significant difference in learning in rats, but it significantly improved memory, significantly reduced malondialdehyde, significantly reduced oxygen free radical levels and significantly reduced activity. Acetylcholinesterase and it can be said that berberine with antioxidant properties improved memory and neuroprotection against neurotoxicity caused by aluminum chloride.

Protective effects of L-arginine against aluminium chloride-induced testicular damage in rats.

Aluminium (Al) is a toxic metal with frequent exposure because it is a common element in nature and is found in many products used in daily life. L-arginine is a semi-essential amino acid that is involved in many biochemical pathways in the body and has antioxidant effects. The current research evaluated the possible protective effects of L-arginine against aluminium chloride (AlCl3 ) induced testicular damage. In this animal-based experimental study, 28 male Wistar Albino rats were separated into four groups: control, Al (20 mg/kg/day Al), Al + L-arginine (20 mg/kg/day Al + 50 mg/kg/day L-arginine), and L-arginine (50 mg/kg/day L-arginine). All applications were carried out intraperitoneally (i.p.) for 4 weeks. The histopathological changes caused by exposure to Al in the testicular tissue and the protective effects of L-arginine were investigated by using biochemical, histochemical, immunohistochemical [4-hydroxynonenal (4-HNE) and 8-hydroxy-2'-deoxyguanosine (8-OHdG)] and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay techniques. The testicles in the AlCl3 group showed increased 4-HNE, 8-OHdG expressions, apoptotic index, and abnormal sperm content, while serum testosterone levels, sperm motility, and sperm number were decreased (p < 0.05). Furthermore, histomorphometric examinations of testicular tissue indicated significant structural impairments such as vacuolization in the seminiferous tubule epithelium, edema, and vascular congestion in the interstitial area (p < 0.05). However, the structural alterations were largely ameliorated in the Al + L-arginine group (p < 0.05). Thus, L-arginine, which is an antioxidant, may protect against the harmful effects of Al and may help improve male fertility.

Anti-alzheimer’s Disease Potential of Arabian Coffee Versus Date Palm Seed Extract in Male Rats

Abstract Objectives Utilizing the aluminum chloride rat model for AD to compare the influence of moderately caffeinated (Arabian) and decaffeinated (Date palm seed) coffee on cognitive impairment and pathological events in AD. Methods Twenty Adult Albino male rats of Wistar strain (230 ± 20 g) were divided 4 groups: Group 1: Rats received vehicle and termed as Negative control (NC) group. • Group 2: Rats received Aluminum chloride (10 mg/kg bw, i.p) for 3 weeks (Khan et al., 2013b), starting from 6th to 26th day to induce AD. They were left un-treated and termed as AlCl3 group. • Group 3: Rats were treated intraperitoneally with AlCl3 (10 mg/kg bw) + Arabian coffee aqueous extract (240 mg/kg bw/day, p.o) for 2 weeks (Jang et al., 2013), starting from the 27th day and termed as AlCl3 + Arabian coffee group. This dose is nearly equivalent to human consumption of 6 cups of coffee. • Group 4: Treated intraperitoneally with AlCl3 (10 mg/kg bw) + standardized extract of Date Palm seed dried powder (240 mg/kg bw/day, p.o) for 2 weeks, starting from the 27th day and termed as AlCl3 + Date seed extract group. Results AD rats given Arabian or Date palm seed coffee were protected against memory impairment and had lower serum levels of the abnormal protein (amyloidbeta; Aβ1–42), the central pathogenic contributor to AD, and transforming growth factor-beta (TGF-β). Interestingly, Date palm seed (decaffeinated) coffee seems to provide more pronounced protection against AD than Arabian (moderately caffeinated) coffee as evidenced by the greater decrease in serum Aβ levels. These results suggest a surprising therapeutic potential of moderate caffeine intake in Arabian coffee to ameliorate AD through decreasing serum Aβ levels. However, Date palm seed (decaffeinated) coffee, rich in flavonoids, appears to provide a better AD-modifying ability through a direct reduction of Aβ production. Conclusions Consumption of Arabian coffee containing moderate caffeine seems to ameliorate AD-induced cognitive impairment via decreasing Aβ levels. Interestingly, intake of decaffeinated Date seed extract, rich in flavonoids, appears to provide a superior anti-AD potential through a direct reduction of Aβ production. Funding Sources No funding.

Amelioration of aluminum-induced hepatic and nephrotoxicity by Premna odorata extract is mediated by lowering MMP9 and TGF-β gene alterations in Wistar rat

This study aims to investigate the effect of Premna odorata (P. odorata) (Lamiaceae) on the hepatic and nephrotoxicity induced by aluminum chloride (AlCl3) in rat. Wistar male rats were equally classified into four groups: control, P. odorata extract (500 mg/kg B.W.), AlCl3 (70 mg/kg B.W.), and P. odorata extract plus AlCl3 groups. All treatments were given orally for 4 weeks. Serum transaminases and some biochemical parameters, hepatic and renal antioxidant/oxidant biomarker; tumor necrosis factor-α (TNF-α); matrix metalloproteinase (MMP9) and transforming growth factor-β (TGF-β) mRNA expression; histopathological examination of the liver, and kidneys were investigated. The obtained results revealed that AlCl3 significantly increased the activities of serum aspartate transaminase, alanine transaminase, and alkaline phosphatase as well as produced a significant increase in total cholesterol, triglyceride, urea, and creatinine concentrations, while there were no changes observed in the total protein, albumin, and globulin concentrations. Also, aluminum administration significantly decreased the reduced glutathione content and increased the catalase activity, malondialdehyde, and TNF-α concentrations in the liver and kidney tissue. Moreover, AlCl3 results in congestion, degeneration, and inflammation of the liver and kidney tissue. Co-treatment of P. odorata extract with AlCl3 alleviated its harmful effects on the previous parameters and reduced the histopathological alterations induced by AlCl3. Therefore, Premna odorata may have a potent protective effect against oxidative stress induced by Al toxicity through downregulation of MMP9 and TGF-β gene expression.

Celastrol and thymoquinone alleviate aluminum chloride-induced neurotoxicity: Behavioral psychomotor performance, neurotransmitter level, oxidative-inflammatory markers, and BDNF expression in rat brain

Exposure to aluminum chloride (AlCl3) induces progressive multiregional neurodegeneration in animal models by promoting oxidative stress and neuroinflammation. The current study was designed to assess the potential efficacy of the natural antioxidants celastrol and thymoquinone (TQ) for alleviating AlCl3-induced psychomotor abnormalities and oxidative-inflammatory burden in male albino rats. Four treatment groups were compared: (i) a vehicle control group, (ii) a AlCL3 group receiving daily intraperitoneal (i.p.) injection of AlCl3 (10 mg/kg) for 6 weeks, (iii) a AlCl3 plus TQ (10 mg/kg, i.p.) cotreatment group, and (iv) a AlCl3 plus celastrol (1 mg/kg, i.p.) cotreatment group. Open-field, rotarod, and forced swimming tests were conducted to assess locomotor activity, motor coordination, anxiety-like behavior, and depressive-like behavior. Acetylcholine (ACh), dopamine, and serotonin levels were measured in brain homogenates. Malondialdehyde (MDA), total antioxidant capacity (TAC), and catalase activity were measured as oxidative stress markers, while tumor necrosis factor-α (TNF-α) and interlukin-6 (IL-6) expression levels were measured as inflammatory markers. Brain derived neurotrophic factor (BDNF) mRNA was measured as an index for the endogenous neuroprotective response. Daily AlCl3 injection reduced free ambulation, impaired motor coordination, promoted anxiety- and depression-like behaviors, reduced whole-brain ACh, dopamine, and serotonin concentrations, increased MDA accumulation, reduced TAC, elevated TNF-α and IL-6, and suppressed BDNF mRNA expression. All of these effects were significantly reversed by TQ or celastrol cotreatment. Thus, TQ and celastrol may be promising treatments for AlCl3-induced neurotoxicity as well as neurodegenerative diseases involving oxidative stress and neuroinflammation.

Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine

Aluminum, the third most plentiful metal in the Earth’s crust, has potential for human exposure and harm. Oxidative stress plays an essential role in producing male infertility by inducing defects in sperm functions. We aimed to investigate the role of endoplasmic reticulum (ER) stress and mitochondrial injury in the pathogenesis of aluminum chloride (AlCl3)-induced testicular and epididymal damage at the histological, biochemical, and molecular levels, and to assess the potential protective role of taurine. Forty-eight adult male albino rats were separated into four groups (12 in each): negative control, positive control, AlCl3, and AlCl3 plus taurine groups. Testes and epididymis were dissected. Histological and immunohistochemical (Bax and vimentin) studies were carried out. Gene expression of vimentin, PCNA, CHOP, Bcl-2, Bax, and XBP1 were investigated via quantitative real-time polymerase chain reaction (qRT-PCR), besides estimation of malondialdehyde (MDA) and total antioxidant capacity (TAC). Light and electron microscopic examinations of the testes and epididymis revealed pathological changes emphasizing both mitochondrial injury and ER stress in the AlCl3 group. Taurine-treated rats showed a noticeable improvement in the testicular and epididymal ultrastructure. Moreover, they exhibited increased gene expression of vimentin, Bcl-2, and PNCA accompanied by decreased CHOP, Bax, and XBP1 gene expression. In conclusion, male reproductive impairment is a significant hazard associated with AlCl3 exposure. Both ER stress and mitochondrial impairment are critical mechanisms of the deterioration in the testes and epididymis induced by AlCl3, but taurine can amend this.

The effects of aqueous leaf extract of Portulaca oleracea on haemato-biochemical and histopathological changes induced by sub-chronic aluminium toxicity in male wistar rats

BackgroundPurslane has wide acceptability as a potherb in Central Europe, Asia, and Mediterranean region, it is very used in traditional Chinese medicine (TCM) to treat fever, dysentery, diarrhea, carbuncles, eczema, and to remove toxic substances. Our study aimed to investigate the impact of purslan on physiological and biochemical alterations induced by AlCl3 intoxication in rats. MethodologyFifteen males albino Wistar rats were randomly divided into 3 groups (n = 5); healthy rats (Control), AlCl3 (200 mg/kg b.w) treated rats and AlCl3 (200 mg/kg b.w) rats treated with aqueous extract of P. oleracea (400 mg/kg b.w). AlCl3 treatments were given to rats orally for 70 days and purslan extract for 21 days. Various parameters as hematological, biochemical, oxidative stress markers and liver histopathology were estimated. In-vitro study of plant, some quantitative parameters was analyzed using standard protocols. ResultsIn vitro phytochemical test results revealed that purslane contains most of the principal active molecules, especially flavonoids and phenolic compounds. In vivo results, the AlCl3 group showed an alteration in the antioxidant defend system by increasing the MDA level and decreasing the GSH levels, GST and SOD activities compared to control. Furthermore, the hematological parameters revealed that AlCl3 induce an inflammation in rats by significant raise (P<0.01) of WBC, Monocyte, LYM and platelet (P<0.001) levels with a significant perturbation in lipid profile and biochemical parameters. In the other hand, histopathological analysis recorded a deep modification in liver tissues of AlCl3 rats group compared to control. However, the treatment of AlCl3 rats by purslan ensured a partial amelioration and correction of the previous parameters. ConclusionWe conclude that the use of purslane seems to be the powerful limited of AlCl3 toxicity development, which opening the new horizons for the use of phytotherapy in medical approach.

Comparison anti-oxidant and neuroprotective effects of extra-virgin olive oil, donepezil and rosmarinic acid on aluminum chloride-induced Alzheimer’s in rat models

In this study, it was aimed to investigate the effects of EVOO, rosmarinic acid and donepezil in Alzheimer's model to be created with AlCl3 in rats. For this reason, administration of 100 mg/kg aluminum chloride (AlC3) for 15 days to Sprague Dawley adult male rats; donepezil, Extra-virgin olive oil (EVOO) and rosmarinic acid were administered to three different groups for 21 days by applying treatment protocols. With this study, we were able to demonstrate that cognitive impairment has been occurred after 15 days of AlCl3 administration by oral gavage and treatment protocols prevented the occurrence of AD pathology histopathologically. We also showed that oxidative damage findings which are positively Congo-red stained cell cytoplasm and impaired cell integrity have been observed in serum and hippocampus. Besides, treatment groups showed better cognitive and motor performance, and there was no damage to the cells in control and treatment groups. In the rotarod motor performance test, a significant increase was observed in the donepezil group compared to the AlCl3 group at speeds of 26 and 30 rpm. In MVM, on the 5th day of the experiment, a significant increase was observed in the donepezil group compared to the AlCl3 group, as they were spending more time in the hidden platform area. These results show that 15 days of aluminum exposure is effective in creating a moderate Alzheimer’s pathology, but further chronic research is necessary to explain the efficiencies of rosmarinic acid and EVOO in treatment.

Cognitive, Anticholinesterase and Anti-Oxidative Potentials of Zingiber officinale Rhizome Extracts against Aluminium Chloride- Induced Neurotoxicity in Swiss Mice

Aluminium neurotoxicity is implicated in Alzheimer's disease, which is marked by progressive memory loss, cognitive impairment and structural degeneration, leading to complete incapacitation. Formation of excess reactive oxygen species causes oxidative stress, which is the hallmark of aluminium toxicity. A quest to counteract these pathologies led to investigating Zingiber officinale (ZO) extracts on cognitive and anti-oxidative potentials against aluminium chloride (AlCl3)-induced neurotoxicity in Swiss mice. The oral lethal dose of ZO was estimated as 4,743 mg/kg. Forty-eight adult female Swiss mice of weight 21-27 g were then assigned to eight groups (n=6): Group 1 were the control (40 mL/kg distilled water), while groups 2-8 were respectively, administered AlCl3 (100 mg/kg) alone, and with Donepezil (2.5 mg/kg), ZO ethanol extract (474, 949 and 1,423 mg/kg), ZO dichloromethane (949 mg/kg), and ZO methanol (949 mg/kg) extracts for 21 days. The classic labyrinth test was carried out subsequently, the animals sacrificed, and their brain homogenized for biochemical assay. There was a significantly (p&lt;0.05) increased latency to complete the labyrinth test by the AlCl3 group compared with the control. The ZO extracts treated groups had decreased latency to complete the labyrinth test, and these were significant (p&lt;0.05) in the 949 and 1,423 mg/kg ethanol extract groups. Biochemically, AlCl3 significantly (p&lt;0.05) elevated acetyl cholinesterase and malondialdehyde levels, while reducing superoxide dismutase activity: These adverse effects were reversed significantly (p&lt;0.05) following treatment with extracts of ZO. In conclusion, ZO ethanol extract and its dichloromethane and methanol fractions improved cognitive activities, and possessed anticholinesterase, anti-oxidant and neuroprotective potentials.

Neuroprotective effect of Bryophyllum pinnatum flavonoids against aluminum chloride-induced neurotoxicity in rats

Toxic metals such as aluminum accumulation in the brain have been associated with the pathophysiology of several neurodegenerative disorders. Bryophyllum pinnatum leaves contain a vast array of polyphenols, particularly flavonoids, that may play a role in the prevention of toxic and degenerative effects in the brain. This study assessed the neuro-restorative potential of leaves of B. pinnatum enriched flavonoid fraction (BPFRF) in aluminum-induced neurotoxicity in rats. Neurotoxicity was induced in male Wistar rats by oral administration of 150 mg/kg body weight of aluminum chloride (AlCl3) for 21 days. Rats were grouped into five (n = 6); Control (untreated), Rivastigmine group, AlCl3 group and BPFRF group (50 and 100 mg/kg b.wt.) for 21 days. Neuronal changes in the hippocampus and cortex were biochemically and histologically evaluated. Expression patterns of acetylcholinesterase (AChE) mRNA were assessed using semi-quantitative reverse-transcription-polymerase chain reaction protocols. Molecular interactions of BPFRF compounds were investigated in silico. The results revealed that oral administration of BPFRF ameliorated oxidative imbalance by augmenting antioxidant systems and decreasing lipid peroxidation caused by AlCl3. BPFRF administration also contributed to the down-regulation of AChE mRNA transcripts and improved histological features in the hippocampus and cortex. Molecular docking studies revealed strong molecular interactions between BPFRF compounds, catalase, superoxide dismutase and glutathione peroxidase Overall, these findings suggest the neuroprotective effect of Bryophyllum pinnatum against aluminum-induced neurotoxicity.

Effect of quercetin as therapeutic and protective agent in Aluminum Chloride-induced Alzheimer's disease rats

Alzheimer's disease (AD) is a neurodegenerative disease clinically characterized by progressive cognitive impairment. This work aimed to investigate the role of quercetin (Q) in the treatment and protection of AlCl3-induced AD in rats through exploring the molecular mechanisms underlying its neuroprotective and therapeutic properties. In this study, male Wistar rats were allocated to two experiments: experiment I (therapeutic effect of quercetin) in which the rats were divided into: normal control group (C-Saline) which was induced with saline for 56 days, C-Q50 group, which was administered orally with Q (50 mg/kg) for 28 days after induction saline for 28 days, AD (AlCl3-Saline) group received AlCl3 (50 mg/kg) intraperitoneally for 28 days followed by saline for 28 days, and the AlCl3-Q50 group received Q (50 mg/kg) orally for 28 days after induction with AlCl3 for 28 days. In experiment II rats were divided into: normal control (NC) group, Q50 (50 mg/ kg) group, AlCl3 (AD) group, and AlCl3 + Q50 group which was co-administrated with AlCl3 + Q50 for 56 successive days. Dopamine (DA) and acetylcholinesterase) AChE (levels were estimated for all rat groups. The results showed that post-treatment of the AD-induced rats with Q50 as well as co-administration of AlCl3with Q50, significantly reduced the AChE level in serum, significantly increased the DA level, and significantly increased the body weight change compared to the AlCl3group, but did not show any significant change in the brain weight. We concluded that quercetin significantly improved the cholinergic and dopaminergic dysfunctions by lowering the Acetylcholine esterase level and restoring the dopamine level

Pomegranate juice moderates anxiety- and depression-like behaviors in AlCl3-treated male mice

PurposeAluminum trichloride (AlCl3) exposure was proven to encourage some behavioral deficits and eventually induces anxiety and depression in rodents animals. Therefore, this experiment aimed to scout about the effects of pomegranate juice on anxiety- and depression-like behaviors caused by AlCl3 in male mice. MethodsSix groups of male mice were administrated orally for 35 days by PJ and AlCl3. The control group (G-I) received tap water, while the PJ groups (G-II and G-III) were treated with 20 % and 40 % PJ, respectively. The AlCl3 group (G-IV) was treated with 400 mg/kg/day of AlCl3, and the last two groups (G-V and G-VI) were treated with AlCl3 and 20 % PJ or 40 % PJ, respectively. Then, the open-field (O-F), elevated plus maze (EPM), tail suspension (TS), forced swimming (FS), and light/dark box (L/DB) tests were applied for anxiety- and depression-like behavior studies. In addition, neurotransmitters and oxidative parameters in the brain were evaluated. The plasma cortisol was measured at the end of the experiment. ResultsBehavioral analyses showed that PJ inhibited AlCl3-induced depressive and anxiogenic effects in the O-F, EPM, TS, FS, L/DB tests. In addition, neurochemical results indicated that PJ at 20 % concentration minimized the AlCl3 toxicity on dopamine (DOP), serotonin (SER), and acetylcholinesterase (AChE) levels in the for-brain of male mice. Moreover, PJ moderated the AlCl3 effects by decreasing the level of thiobarbituric acid reactive substances (TBARS), and enhancing catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST) and glutathione (GSH) activities. The plasma cortisol increased in male mice treated with AlCl3 and in a group treated with a high dose of PJ. ConclusionOur results proposed that the anxiety- and depression-like behaviors induced by AlCl3 exposure in male mice can be ameliorated by PJ treatment, probably through the inhibition of oxidative damage and minimizing the changes in neurotransmitters and hormonal activity.

Rhamnus alaternus aqueous extract enhances the capacity of system redox defence and protects hepatocytes against aluminum chloride toxicity in rats

BackgroundThis study was designed to evaluate the protective effects of a Rhamnus alaternus aqueous extract (RAAE) on aluminum chloride-induced hepatotoxicity in rats. A preliminary phytochemical study and antioxidant activity tests of the extract were performed.MethodsA preliminary phytochemical study and antioxidant activity tests of the extract were performed. For the in vivo study, twenty-four male rats were divided into four groups. The control group (C); the RAAE group treated with 250 mg/kg b.w RAAE; the AlCl3 group, which received 50 mg/kg b.w AlCl3; and the AlCl3/RAAE group that was treated with AlCl3 plus RAAE.ResultsThe RAAE contains several phenolic compounds. This plant extract showed a high radical scavenging effect and high antioxidant activity. Administration of AlCl3 resulted in a significant increase in the activities of aspartate aminotransferase and alanine aminotransferase (AST, ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) and significant decreases in the plasma concentrations of total proteins and albumin. Moreover, AlCl3 induced a hepatic pro-oxidant effect leading to an increase in malonaldehyde (MDA) and carbonyl protein contents, the depletion of the content of reduced glutathione (GSH) and a decrease in the antioxidant enzymatic activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). However, RAAE supplementation with AlCl3 treatment significantly decreased the levels of MDA and carbonyl proteins and markedly restored the activities of the antioxidant enzymes. These results are supported by the improvement in liver tissue restoration.ConclusionsThe Rhamnus alaternus aqueous extract was shown to have effective antioxidant activity owing to its phenolic compounds protecting against AlCl3-induced liver oxidative damage.

The Effects of Cannabis sativa L. Extract on Oxidative Stress Markers In Vivo.

In recent decades, a lot of attention has been paid to Cannabis sativa L. due to its useful applications, including in fibers, oil, food for humans and animals, and therapeutics. The present study aimed to determine antioxidant activity of cannabinoids in Cannabis sativa L. in vivo, evaluating the possible antioxidative effect of Cannabis sativa L. extract (CE) on malondialdehyde (MDA) and glutathione (GSH) concentrations as well as on catalase (CAT) activity in BALB/c mice. In total, 40 mice were divided into five equal groups: the aluminum group (7.5 mg AlCl3/kg/d (0.15 LD50), the saline group, the 10% ethanol group (an appropriate amount of the solution for mouse weight), the CE group (1.6 mg CE/g/day), and the aluminum-CE group (7.5 mg AlCl3 plus 1.6 mg CE/g/day). The results of the study showed that CE significantly decreased (by 26.81%, p < 0.05) the concentration of GSH in blood of the mice and the concentration of MDA in the brain (by 82.12%) and liver (by 53.5%) of the mice compared to the respective concentrations in the AlCl3 group. CE significantly (p < 0.05) increased CAT activity in the brain (by 64.79%) and liver (by 72.37%) of the mice after the AlCl3-induced prooxidant effect. The results showed the antioxidant activity of cannabidiolic acid (CBDA) in vitro. The findings in vivo indicate that Cannabis sativa L. is a good source of natural antioxidants and can be used in the management of oxidative stress.

Pomegranate juice reverses AlCl3-Induced neurotoxicity and improves learning and memory in female mice

BackgroundAluminum is a neurotoxic element that can accumulate in the brain and cause neurodegenerative disorders. In addition, the antioxidants found in pomegranate juice (PJ) are much more than those existing in other fruits. It was proven to provide protection against neurodegenerative diseases. ObjectivesThis experiment aimed to clarify the amelioration efficiency of PJ against aluminum chloride-induced neurobehavioral and biochemical disorders in female mice. MethodsThe female mice were given oral administrations for 35 days as follows. The control group received tap water, the PJ groups received 20% and 40% pomegranate juice, the aluminum chloride (AlCl3) group was treated with 400 mg/kg AlCl3, and the last two groups received AlCl3 + 20% PJ and AlCl3 + 40% PJ, respectively. The neurobehavioral features were assessed by shuttle box, T-maze, and Morris water maze devices. Furthermore, the neurotransmitters and oxidative indicators in the brains of the female mice were determined at the end of experiment. ResultsSignificant effects of AlCl3 were observed on female mice in the body weight, during the behavioral tasks (shuttle box, T-maze, and Morris water maze), and in neurotransmitters and oxidative stress parameters. Pomegranate juice, especially at low concentrations, induced remarkable improvements in body weight, spatial memory and learning during T-maze, Morris water maze and shuttle box tasks, as well as in neurotransmitters and oxidative biomarkers in the AlCl3-treated female mice. ConclusionPJ reversed AlCl3-induced neurotoxicity and improved learning and memory in female mice. However, PJ contains a group of antioxidants that may be considered double-edged swords in the cellular redox status especially at high doses.

Aluminum Chloride-Induced Oxidative Damage to Serum and Combined Intervention of Ascorbic Acids and Massularia Acuminata On Selected Markers Of In Vivo Antioxidant Enzymes in Wistar Rats

This study evaluates the synergistic antioxidants effects of extracts of Massularia acuminata and ascorbic acid in aluminum chloride-treated oxidative stress in wistar albino rats with a view to investigate the preventive potential of co-administration of Massularia acuminata and ascorbic acids. The in vivo antioxidant properties of the extract were evaluated using in vivo catalase activity, superoxide dismutase activity and thiobarbituric acid reactive substances assay by standard methods via spectrophotometry. The in vivo studies were carried out on rats, grouped majorly into positive control, negative control and the treated groups. The positive control group was administered with normal saline (distilled water) orally, while the negative control group was orally induced with the toxicant (aluminium chloride). The treated group was orally administered with the extract after toxicant administration. Ascorbic acid was used as standard antioxidant in the study. The effects on enzymatic antioxidants and lipid indices were evaluated. Forty healthy Wistar rats sub-grouped into ten (10) groups were induced with aluminum chloride. Some rats were treated with ascorbic acid which is a well-known antioxidant, while others were treated with various extracts of Massularia acuminata (Pako Ijebu) at various doses. The experiment is designed as follows: in Group 1, animals were used as control group. Animals in Group 2 were the toxicant-treated groups administered with AlCl3 (34 mg/kg body weight). Ascorbic acid treated groups are the standard control (group 3) administered with 200 mg/kg body weight. Animals in Group 4 were co-treated with AlCl3 and Ascorbic acid (34 mg/kg aluminum chloride and 200 mg/kg body weight of ascorbic acid). Animals in group 5 were co-administered with ethanolic extract (50 mg/kg body weight) of Massularia acuminata and AlCl3 (34 mg/kg body weight), respectively. Animals in group 6 were also co-treated and administered with ethanolic extract of Massularia acuminate (100 mg/kg body weight) and AlCl3, respectively. Experimental animals in group 7 were equally co-administered with methanolic extract of Massularia acuminate (50 mg/kg body weight) and AlCl3, respectively. Animals in group 8 were co-administered with methanolic extract of Massularia acuminate (100 mg/kg body weight) and AlCl3, respectively. Group 9 animals were co-administered with butanolic extracts of Massularia acuminata (50 mg/kg body weight) and AlCl3, respectively. Group 10 experimental animals were also co-administered with butanolic extract of Massularia acuminate (100 mg/kg body weight) and AlCl3, respectively. At the end of the experiment, the animal was sacrificed after three weeks by cervical dislocation after they were immobilized using chloroform. Results show that ethanolic and methanolic extracts of Massularia acuminata contain antioxidant properties. Both doses of ethanolic extract dose (50 mg/kg and 100 mg/kg body weight) group of methanol extract also reduced the level of MDA but not as ascorbic acid group. Both doses of methanolic extract of Masssularia acuminata act contrariwise from other extracts in that they show the highest level of malonaldehyde even more than AlCl3. The results of superoxide dismutase (SOD) assay test in this study show that the control group, ascorbic acid combined with AlCl3 group, 50 mg/kg body weight of ethanolic extract. Both doses of methanolic extract groups have the same comparative value of SOD. The group treated with toxicant (aluminum chloride) and ascorbic group has similar relative value. The group treated with 50 mg/kg body weight of butanolic extract shows the highest value of superoxide dismutase activity that follow closely by 100 mg/kg of ethanolic extract group. The study concluded that Massularia acuminata, like ascorbic acids, can induced antioxidant enzymes such as SOD and CAT in aluminium chloride-induced oxidative stressed rats. It may therefore be used to protect the body against any pathological attacks from free radical and oxidative insults.

Long-term exposure to low doses ofaluminumaffects mineral content and microarchitecture of rats alveolar bone.

Aluminum (Al) is one of the most found elements in nature in many forms, and human exposure can be quite common. Therefore, it is important to investigate the effects of exposure to Al mainly atlow doses and for a prolonged period, in order to simulate human exposure in the periodontium, an important structure forsupport and protection of the teeth. This investigation aimed to study the aluminum chloride (AlCl3) toxicological effects in the mineral composition and micromorphology of the alveolar bone of rats. Two groups of eight male Wistar rats were used for the experiment. AlCl3 group was exposed to AlCl3 orally at a dose of 8.3 mg/kg/day for 60 days, while the control group received only distilled water. After that, the mandibles were collected and submitted to the followinganalyses: Fourier transform infrared spectroscopy, Raman spectroscopy, and X-ray microtomography analysis; blood was also collected for determination of Al circulating levels. Our data showed that AlCl3 was capable of increasing Al circulating levels in blood. It was able to promote changes in the mineral content and triggers significant changes in the mineralized bone microstructure, such as number and thickness of trabeculae, being associated with alveolar bone-loss.

Protective Effects of 3-benzoyl-7-hydroxy Coumarin on Liver of Adult Rat Exposed to Aluminium Chloride

In this study, the effects of 3-benzoyl-7-hydroxy coumarin molecule on mineral and antioxidant enzymes were investigated in rat liver exposed to oxidative stress with aluminium chloride (AlCl3). Adult male Wistar albino rats were divided into four groups as Control, Coumarin, AlCl3, and Coumarin + AlCl3. Coumarin at the dose of 10 mg / kg and AlCl3 at the dose of 8.3 mg / kg were administered for 30 days every other day. In AlCl3 group, malondialdehyde (MDA), iron (Fe), aluminium (Al) and copper (Cu) levels increased compared to the control group, while glutathione (GSH) level, glutathione S-transferase (GST), and carboxylesterase (Ces) enzyme activity levels decreased. In Coumarin + AlCl3 group, MDA, Fe, Al and Cu levels decreased with the effect of coumarin compared to AlCl3 group, while GSH level, and GST enzyme activity levels increased. According to our results, AlCl3 generates oxidative stress in rat livers, and we believe that 3-benzoyl-7-hydroxy coumarin has an ameliorative effect on antioxidant enzyme system, Al, Fe and Cu levels.

The protective effect of esculetin against aluminium chloride-induced reproductive toxicity in rats.

One of the prominent health problems caused by Aluminium was the decrease in male fertility rates. In the study, the protective effect of Esculetin (ESC) against the reproductive toxicity induced by Aluminium chloride (AlCl3 ) was investigated. For this purpose, AlCl3 was administrated to Wistar Albino rats at a dose of 34mg/kg and ESC was administrated at a dose of 50mg/kg for 70days. It was determined that AlCl3 treatment reduced sperm motility and concentration, increased dead/live rate and abnormal sperm rate. It decreased serum testosterone level, and co-treatment of ESC significantly regulated these values. In the AlCl3 -treated group, MDA level increased and GSH level, GPx and CAT activities decreased compared with those of the control group. However, co-treatment of ESC showed an amelioratory effect on the values except for CAT activity. It was observed that the expression level of NRF-2 increased in the ESC and AlCl3 +ESC groups, and NF-κB increased in the AlCl3 group with the control group. It was determined that Caspase-3 expression decreased, and Bcl-2 expression increased in AlCl3 +ESC group compared to AlCl3 group. It was also determined that AlCl3 -induced tissue injury was significantly prevented by ESC co-treatment.

Effect of Moringa oleifera Lam. Leaf Extract Against Aluminium Chloride Induced Hippocampal Histology and Serum Enzyme activities in adult Wistar rats

Introduction: Aluminium, a ubiquitous metal implicated in some neurodegenerative diseases is linked to activation of free oxygen species. The antioxidant-rich plants, Moringa oleifera (MO) is reported to protect against Aluminium activities. This study investigated the actions of MO leaf extract (MOLE) against Aluminium chloride (AlCl3 )- induced hippocampal cellular changes and serum levels of alkaline phosphatase (ALP), aspartate transaminase (AST) and alanine transaminase (ALT) in adult Wistar rats. Materials and Methods: Thirty Wistar rats weighing between 150 g and 220 g were grouped (n=5) into; 1-control (5 mL/kg distilled water), 2-AlCl3 (100 mg/kg), 3-low dose MOLE (250 mg/kg), 4-high dose MOLE (1,000 mg/kg), 5-concurrent AlCl3 and low dose MOLE, and 6-concurrent AlCl3 and high dose MOLE. All administrations were by oral gavages for 21 days. On day 22, following deep anaesthesia and cardiac puncture, blood was obtained for serum enzyme analysis, and the brain perfusion fixed, harvested and processed for histological study. Results: Results showed significantly (p &lt; 0.05) higher ALP level in the AlCl3 group compared with the control, as well as the other test groups. However, there was no significant (p &gt; 0.05) AST and ALT levels. The hippocampal CA3 of the AlCl3 group showed hypertrophic cells, with some of the cells having karyorrhectic features. The concurrent AlCl3 and low and high doses, MOLE groups showed less of these adverse features. Conclusion: These results suggest that MOLE may protect enzymatic activities against Aluminium chloride. However, its action on hippocampus is still subject to further investigation.