Increase In MDA Levels Research Articles

Soybean isoflavones alleviate cerebral ischemia/reperfusion injury in rats by inhibiting ferroptosis and inflammatory cascade reaction

To explore the mechanism that mediates the effect of soybean isoflavones (SI) against cerebral ischemia/reperfusion (I/R) injury in light of the regulation of regional cerebral blood flow (rCBF), ferroptosis, inflammatory response and blood-brain barrier (BBB) permeability. A total of 120 male SD rats were equally randomized into sham-operated group (Sham group), cerebral I/R injury group and SI pretreatment group (SI group). Focal cerebral I/R injury was induced in the latter two groups using a modified monofilament occlusion technique, and the intraoperative changes of real-time cerebral cortex blood flow were monitored using a laser Doppler flowmeter (LDF). The postoperative changes of cerebral pathological morphology and the ultrastructure of the neurons and the BBB were observed with optical and transmission electron microscopy. The neurological deficits of the rats was assessed, and the severities of cerebral infarction, brain edema and BBB disruption were quantified. The contents of Fe2+, GSH, MDA and MPO in the ischemic penumbra were determined with spectrophotometric tests. Serum levels of TNF-α and IL-1βwere analyzed using ELISA, and the expressions of GPX4, MMP-9 and occludin around the lesion were detected with Western blotting and immunohistochemistry. The rCBF was sharply reduced in the rats in I/R group and SI group after successful insertion of the monofilament. Compared with those in Sham group, the rats in I/R group showed significantly increased neurological deficit scores, cerebral infarction volume, brain water content and Evans blue permeability (P < 0.01), decreased Fe2+ level, increased MDA level, decreased GSH content and GPX4 expression (P < 0.01), increased MPO content and serum levels of TNF-α and IL-1β (P < 0.01), increased MMP-9 expression and lowered occludin expression (P < 0.01). All these changes were significantly ameliorated in rats pretreated with IS prior to I/R injury (P < 0.05 or 0.01). SI preconditioning reduces cerebral I/R injury in rats possibly by improving rCBF, inhibiting ferroptosis and inflammatory response and protecting the BBB.

Removal of lithium from aqueous solutions by solid-phase extraction using sawdust loaded with magnetite nanoparticles and study of apoptosis, MDA and 8-OHdG caused by lithium toxicity in fish brain.

Lithium, which has a high industrial value, is an environmental pollutant of concern to those who work with lithium in industry as well as to the general public. Biological parameters such as MDA, 8-OHdG, apoptosis (caspase-3), and acetylcholinesterase (AChE) were studied to determine the toxic effects on the brain tissue of the model organism (Carassius auratus) exposed to high dose lithium. According to the results obtained, it was found that lithium exposure caused oxidative stress with an increase in MDA level over time and, accordingly, DNA damage and apoptosis occured in brain tissue. It was also found that a decrease in AChE activity was observed, and the high levels of MDA, 8-OHdG, and caspase-3 activity obtained in brain tissue supported this result. The solid phase extraction (SPE) method was used to effectively remove lithium, which has unfavorable effects on living organisms, from aqueous solutions. In this method, a sawdust loaded with magnetite nanoparticles (MNLS) was prepared as an adsorbent for solid phase extraction by a simple method, and it was characterized. Optimal conditions for the SPE process were defined and it was found that lithium could be removed from solution onto the MNLS surface with a high yield of about 96%. The results of the study are crucial for proposing a simple and applicable high performance method.

Blue LED light induces cytotoxicity via ROS production and mitochondrial damage in bovine subcutaneous preadipocytes

The purpose of this study was to investigate the effect and mechanism of blue light irradiation on bovine subcutaneous preadipocytes. In this study, preadipocytes were divided into dark group (control) and blue light group. Results show that blue light exposure time-dependently reduced the viability of preadipocytes and induced mitochondrial damage, in accompaniment with the accumulation of intracellular reactive oxygen species (ROS). Meanwhile, blue light caused oxidative stress, as evidenced by the increased MDA level, the reduced T-AOC contents, as well as the decreased activities of antioxidant enzymes. Additionally, blue light treatment induced apoptosis and G2/M phase arrest via Bcl-2/Bax/cleaved caspase-3 pathway and P53/GADD45 pathway, respectively. Protein expressions of LC3-II/LC3-I and P62 were up-regulated under blue light exposure, indicating blue light initiated autophagy but impeded autophagic degradation. Moreover, blue light caused an increase in the secretion of pro-inflammatory factors (TNF-α, IL-1β, and IL-6). Pretreatment with N-acetylcysteine (NAC), a potent ROS scavenger, restored the loss of mitochondrial membrane potential (Δψ) and reduced excess ROS. Additionally, the above negative effects of blue light on cells were alleviated after NAC administration. In conclusion, this study demonstrates blue light induces cellular ROS overproduction and Δψ depolarization, resulting in the decrease of cell viability and the activation of apoptosis, autophagy, and inflammation, providing a reference for the application of blue light in the regulation of fat cells in the future.

Elevated CO2 and temperature under future climate change increase severity of rice sheath blight.

Sheath blight (ShB), caused by Rhizoctonia solani, is one of the major threats to rice (Oryza sativa L.) production. However, it is not clear how the risk of rice ShB will respond to elevated CO2 and temperature under future climate change. Here, we conducted, field experiments of inoculated R. solani under combinations of two CO2 levels (ambient and enriched up to 590 μmol mol-1) and two temperature levels (ambient and increased by 2.0°C) in temperature by free-air CO2 enrichment (T-FACE) system for two cultivars (a susceptible cultivar, Lemont and a resistant cultivar, YSBR1). Results indicate that for the inoculation of plants with R. solani, the vertical length of ShB lesions for cv. Lemont was significantly longer than that for cv. YSBR1 under four CO2 and temperature treatments. The vertical length of ShB lesions was significantly increased by elevated temperature, but not by elevated CO2, for both cultivars. The vertical length of ShB lesions under the combination of elevated CO2 and elevated temperature was increased by 21-38% for cv. Lemont and by -1-6% for cv. YSBR1. A significant increase in MDA level was related to a significant increase in the vertical length of ShB lesions under the combination of elevated CO2 and elevated temperature. Elevated CO2 could not compensate for the negative effect of elevated temperature on yield of both cultivars under future climate change. Rice yield and biomass were further decreased by 2.0-2.5% and 2.9-4.2% by an increase in the severity of ShB under the combination of elevated CO2 and elevated temperature. Thus, reasonable agronomic management practices are required to improve both resistance to ShB disease and grain yield for rice under future climate change.

Exogenous fetuin-A protects against sepsis-induced myocardial injury by inhibiting oxidative stress and inflammation in mice.

Sepsis-induced myocardial injury is a consequence of septicemia and is one of the major causes of death in intensive care units. A serum glycoprotein called fetuin-A is secreted largely by the liver, tongue, placenta, and adipose tissue. Fetuin-A has a variety of biological and pharmacological properties. The anti-inflammatory and antioxidant glycoprotein fetuin-A has shown its efficacy in a number of inflammatory disorders including sepsis. However, its protective role against sepsis-induced myocardial injury remains elusive. The purpose of this work is to explore the role of fetuin-A in mouse models of myocardial injury brought on by cecal ligation and puncture (CLP). CLP significantly induced the myocardial injury assessed in terms of elevated myocardial markers (serum CK-MB, cTnI levels), inflammatory markers (IL-6, TNF-α) in the serum, and oxidative stress markers (increased MDA levels and decreased reduced glutathione) in heart tissue homogenate following 24 h of ligation and puncture. Further, hematoxylin and eosin (H&E) staining showed considerable histological alterations in the myocardial tissue of sepsis-developed mice. Interestingly, fetuin-A pretreatment (50 and 100 mg/kg) for 4 days before the CLP procedure significantly improved the myocardial injury and was evaluated in perspective of a reduction in the CK-MB, cTnI levels, IL-6, and TNF-α in sepsis-developed animals. Fetuin-A pretreatment significantly attenuated the oxidative stress and improved the myocardial morphology in a dose-dependent manner. The present study provides preliminary evidence that fetuin-A exerts protection against sepsis-induced cardiac dysfunction in vivo via suppression of inflammation and oxidative damage.

Impending Chemotherapeutic Impact of Arthrospira platensis Nanoparticles and/or Sorafenib against Hepatocellular Carcinoma through Modulation of Antioxidant Status, Tumor Marker Genes, and Anti-Inflammatory Signaling Pathways.

This study investigated Arthrospira platensis nanoparticles (NSP) to overcome sorafenib resistance in diethyl nitrosamine-induced hepatocellular carcinoma (HCC) in rats. This study used sixty Wistar male rats randomly grouped into two main groups, the normal control group, and the HCC model. For the normal control group (n = 12), animals were injected i.p. with PBS two times/week for 16 weeks. The remaining 48 rats were injected i.p. with using a single dose of diethyl nitrosamine (DENA) (200 mg/kg, ip), followed by phenobarbital sodium (0.05%) in drinking water for 16 weeks. At the end of the 16th week, rats were allocated into four groups (11 rats/each), one group was left without treatment (DENA group), and the other three groups were treated with either sorafenib (30 mg/kg; p.o.) or Arthrospira platensis Nanoparticles (NSP) (0.5 mg/kg body weight) once daily orally with the aid of gastric gavage or their combination for another four weeks. Blood and tissue samples were collected for further biochemical, histological, immunohistochemical, and gene expression analysis. Our result revealed that DENA-treated rats showed a marked elevation of hepatic enzyme markers with an increase in the total protein and globulin and decreases in the hepatic SOD. Catalase and GSH, with significantly increased MDA levels, subsequently increased the tumor biomarkers (AFP and CEA). On the molecular level, the DENA-treated rats showed significant up-regulation of Cyp19 mRNA and the inflammatory cytokines (TNF-α, iNOS, and TGF-1β) as well as the Ki-67 gene expression (p < 0.05) with down-regulation of the PPAR-γ and FOXO-1. In addition, the HCC group showed a loss of hepatic architecture, as well as atypia, swelling, macrosteatosis of hepatocytes, and fibrosis, besides increased vascularization. The immunohistochemical findings show increased expression of both GPC-3 and Hep Par 1 in the HCC group. SOR, NSP, or a combination of NSP and SOR.NSP treatment significantly overturned the DENA's harmful effect near the normal levels and restored all cancer biomarkers and antioxidant activities, indicating the chemotherapeutic impact of NSP. The present study provides evidence that NSP exerts a major anticancer effect on DENA-induced HCC. SOR/NSP is a promising combination for tumor suppression and overcoming sorafenib resistance in HCC by modulating antioxidants, anti-inflammatory signals, and tumor markers.

Unveiling of interactions between foliar-applied Cu nanoparticles and barley suffering from Cu deficiency

The objective of this study was to evaluate nano-Cu-plant interactions under Cu deficiency. Nano-Cu at rates of 100 and 1000 mg L-1 was applied as foliar spray to Hordeum vulgare L. during increased demand for nutrients at tillering stage. Corresponding treatment with CuSO4 was used to exam the nano-specific effects. Cu compounds-plant leaves interactions were analyzed with spectroscopic and microscopic methods (ICP-OES, FTIR/ATR, SEM-EDS). Moreover, the effect of Cu compounds on plants in terms of biomass, pigments content, lipid peroxidation, antiradical properties, the activity of enzymes involved in plant defense against stress (SOD, CAT, POD, GR, PAL, PPO) and the content of non-enzymatic antioxidants (GSH, GSSG, TPC) was determined after 1 and 7 days of exposure. Cu loading to plant leaves increased over time, but the content of Cu under treatment with nano-Cu at 100 mg L-1 was lower by 76% than CuSO4 at 7th day of exposure. The changes induced by applied Cu compounds in biochemical traits were mostly observed after 1 day. Our data showed that CuSO4 exposure induce oxidative stress (increased MDA level and GSSG content) when compared to control and nano-Cu treated plants. Noteworthy, nano Cu at 100 mg L-1 demonstrated enhanced stress tolerance as indicated by boosted GSH content. After 7 days, the antioxidant response was almost same compared to control sample. However, based on other indicators (pigment content, chlorosis sign, biomass), it should be noted that CuSO4 caused serve oxidative burst of plant which may resulted in damage of defense system. Nano-Cu, especially at 100 mg L-1, showed promising effect on plant health, and obtained results may be useful for optimizing of nano-Cu application as fertilizer agent.

Evaluation of ethanol extract of Curcuma longa in lead-induced hippocampal neurotoxicity

Background: Heavy metals such as lead are ubiquitous elements at exposure causing deleterious effects on the brain and leading to neurodegenerative diseases. Aim: In this investigation, the neurotherapeutic effects of ethanol extract of Curcuma longa (EECl) against lead-induced hippocampal neurotoxicity in rats were examined. Biochemical examination for antioxidant enzyme activity and lipid peroxide level (malondialdehyde [MDA], superoxide dismutase [SOD], and glutathione [GSH]) was evaluated, the Barnes maze for learning and memory, and histological analysis (H and E stain) for general histoarchitectural features to investigate the neurotherapeutic characteristics of EECl. Materials and Methods: Six groups totalling 36 rats were created (n = 6). In the first group, rats received distilled water (2 mg/kg), in the second, lead acetate (LA) (120 mg/kg), in the third, ascorbic acid (100 mg/kg), and the 4th, 5th, and 6th groups, rats received LA (120 mg/kg) and EECl (375 mg/kg, 750 mg/kg, and 1500 mg/kg, respectively) for 14 days. Results: A significant learning and memory deficit was seen in the LA-treated group's results, but a significant improvement was seen in the EECl-treated group. Increased oxidative stress was seen in the LA-treated group, as evidenced by an increase in MDA levels and a decrease in antioxidant enzymes (SOD and GSH). A decline in MDA levels and an increase in SOD and GSH activity was the evidence of the ameliorative effects of EECl treatment. Cytoarchitectural distortions relative to the control were observed with the LA-treated group. Mild distortion was however detected with EECl treatment. Conclusion: EECl has possible neurotherapeutic properties against LA-induced pathological changes in the hippocampus of Wistar rats. EECl may have neuroprotective effects against degenerative alterations brought on by LA.

Cerium Oxide Nanoparticles Protect against Oxaliplatin Induced Testicular Damage: Biochemical, Histological, Immunohistochemical, and Genotoxic Study

Oxaliplatin is a chemotherapeutic drug used for colorectal cancer treatment. The testicular toxic effect is one of its recorded toxicities which resulted in a few studies. Oxidative stress could be a direct cause of this testicular toxicity. Cerium oxide nanoparticles (CONPs) are optimistic antioxidants for applications in medicine. The aim of the work is to study the protective effect of CONPs on testicular toxicity induced by oxaliplatin in rats. Forty adult male albino rats were divided into 4 groups: Control group, CONPs group (60 mg/kg, 5 times/week), Oxaliplatin group (4 mg/kg, twice/week), and Oxaliplatin & CONPs group, for 4 weeks. Seventy-two hours after the last administration, blood samples were taken for hormonal levels and testes were used for both histopathology and immunohistochemical microscopic examination. Sperm smears were also performed and their results were statistically analyzed to detect any sperm abnormalities. Oxaliplatin increased MDA levels. SOD and GPx activity was decreased. GSH levels were decreased. Also, it decreased the sperm cell count and serum testosterone, and anti-Müllerian hormon. In the testicular sections, significant histopathology changes were seen and immunohistochemical examination confirmed these results. Upon supplementation of CONPs with oxaliplatin decreased MDA levels. SOD and GPx activity was increased, and GSH did not change. In testicular sections, normal morphology was seen. Also, there was an increase in the sperm cell count and serum testosterone anti-Müllerian with significant improvement of testicular architecture, and immunohistochemical examination confirmed these results. The utilization of CONPs produced significant protection against all of the above-mentioned changes.

Pathological and biochemical investigation of the effects of l-carnitine and gemfibrozil on peroxisome proliferator activated Receptors (PPARS) and lipidosis in rabbits on a high-fat diet

Obesity and fatty liver is a widespread growing health problem in human with detrimental consequences that encouraged researchers to find ways to overcome it. In this study, gemfibrozil and L-carnitine were evaluated in prevention of obesity and hepatic lipidosis also the role of L-carnitine in avoiding side effects of gemfibrozil was investigated. The study involved 56 New-Zealand Albino rabbits, divided into 2 main groups and then subdivided into 4 equal groups (n=7). The groups I (normal diet), II (normal diet+gemfibrozil), III (normal diet+L-carnitine) and IV (normal diet+gemfibrozil+L-carnitine) received normal diet and the groups V (fat rich diet), VI (fat rich diet+gemfibrozil), VII (fat rich diet+L-carnitine) and VIII (fat rich diet+gemfibrozil+L-carnitine) received fat rich diet for 8 weeks. Animals were blood sampled and wieght weekly during the experiment and at the end of the experiment for determination of biochemical (HDL, High-density lipoproteins; LDL, Low-density lipoprotein; VLDL, Very low-density lipoprotein; ALT, Alanine amino transferase; AST, Aspartate aminotransferase; GGT, Gamma glutamyltransferase; GLDH, Glutamate lactate dehydrogenase; LDH, Lactate dehydrogenase) and oxidative stress (MDA, Malondialdehyde; GSH, Reduced gluthation; NO, Nitric oxide; SOD, Superoxide dismutase) parameters. All rabbits were euthanised for histopathological examination and for distrubition of Peroxisome proliferator activated receptors (PPARs) in tissues by immunohystochemistry. Liver enzymes increased in fat rich diet group throughout the study. Addition of gemfibrozil and L-carnitin in fat rich diet resulted in statistically significant decreasein lipid profile when compared to those only received fat rich diet. Beta oxidation of fat rich diet group was significantly higher than that of groups additionally received gemfibrozil and L-carnitine. Immunohistochemistry revealed an increase in PPAR PPAR-α and β but not PPAR-γ expression in fat rich diet group. On the contrary L-carnitin administration did have any effect on tissue PPAR expression. PPAR-α expression differed between groups received gemfibrozil and fat rich diet and those did not. Fat rich diet increased MDA level while decreased GSH and catalase. Addition of gemfibrozil and L-carnitine to fat rich diet significantly decreased MDA level and increased antioxidants. The most marked macroscopy finding was abdominal fat increase in fat rich diet group (group V). On the other hand gemfibrozil administration resulted in significant abdominal fat decrease. Furthermore decreased abdominal fat was marked in gemfibrozil and L-carnitine given animals (group VIII) when compared to other groups. In conclusion, gemfibrozil and L-carnitine administration alleviated abdominal and hepatic fattening and improved lipid profile. Gemfibrozil also caused a significant increase in PPAR-α expression in the liver. It may be of use in avoiding abdominal fat (obesity) due to high fat by use of gemfibrozil, a synthetic PPAR-a ligand, and L-carnitine.

Effects of Flavobacterium psychrophilum extracellular products and lipopolysaccharide antigens on the antioxidant enzyme system activity of rainbow trout (Oncorhynchus mykiss) fry

The aim of this study was to investigate the response of different doses of lipopolysaccharide (LPS) and extracellular product (ECP) antigens (25, 50, 100, 250, and 500 µg) obtained from Flavobacterium psychrophilum to changes in oxidative stress parameters (catalase [CAT], superoxide dismutase [SOD], glutathione peroxidase [GPx], glucose 6-phosphate dehydrogenase [G6PD], glutathione reductase [GR], and malondialdehyde [MDA]) in juvenile rainbow trout. For this purpose, 6 different doses of F. psychrophilum (102–106) were applied to the fish, and the lethal dose 50 % (LD50) value was determined as 1.33·104. Changes in MDA levels and antioxidant enzymes were determined by applying 25 % of the LD50 value to fish for 14 days. Accordingly, while F. psychrophilum increased GR, G6PD, GPx, and SOD activity, it decreased MDA levels and CAT activity. Initially, 25, 50, 100, 250, and 500 µg doses of ECP and LPS were applied to the fish; after 21 days, a 25 % dose of LD50 was applied to these fish. Fourteen days later, the fish were taken, and the changes in MDA levels and antioxidant enzymes were examined. As a result, it was determined that while ECP and LPS application decreased GR, G6PD, GPx, and SOD activity, there was an increase in MDA levels and CAT activity.

Sphaeranthus indicus Linn ameliorates streptozotocin-induced experimental diabetic neuropathy by targeting oxidative stress-mediated alterations

BackgroundDiabetes-induced neuropathic pain is manifested as a lowering of nerve transmission rate, increased discomfort, sensual loss, and axonal degradation, and is the most prevalent secondary consequence of diabetes. Diabetes is a devitalizing disease affecting people from diverse groups in both developing and industrialized countries. The inflammation pathway and oxidative stress both contribute considerably to diabetic peripheral neuropathy via the activation of inflammatory cytokines. Hyperglycemia-mediated neural oxidative stress and damage activates a number of metabolic pathways, causing diabetic neuropathy. The current study investigated the neuroprotective potential of methanolic extract of Sphaeranthus indicus Linn (MESI) in ameliorating diabetic neuropathic pain induced by administration of streptozotocin in rats.ResultsFour weeks after intraperitoneal treatment of streptozotocin (STZ), there was a significant decrease in mechano-tactile allodynia and mechanical and thermal hyperalgesia. Furthermore, STZ-induced oxidative stress increases the extent of neural lipid peroxidation (LPO), as evidenced by increased MDA levels, decreases the activities of endogenous antioxidants such as superoxide dismutase (SOD) and glutathione (GSH), and alters sciatic neural histoarchitecture. Chronic administration of methanolic extract of Sphaeranthus indicus Linn (MESI) for 4 weeks significantly and dose-dependently attenuated the decrease in levels of nociceptive thresholds, endogenous antioxidants (SOD and GSH), and increase in LPO. Furthermore, MESI significantly restored sciatic neural histoarchitecture.ConclusionThe amelioration of streptozotocin-induced diabetic neuropathy by methanolic extract of Sphaeranthus indicus Linn (MESI) could be attributed to its antinociceptive, antioxidant, and neuroprotective properties.

The Oil Formulation Derived from Moringa Oleifera Seeds Ameliorates Behavioral Abnormalities in Water-immersion Restraint Stress Mouse Model.

Repeated stress events are well known to be associated with the onset of behavioral abnormalities including depression, anxiety and memory impairment. In spite of the traditional uses of Moringa oleifera (MO), no experimental evidence for its use against chronic stress exists. Here, we investigated whether seed oil from MO (MOO) could improve behavior abnormalities of chronic stress mice induced by water-immersion restraint stress (WIRS) and the underlying mechanism. BALB/C male mice at 12 weeks of age were exposed to chronic WIRS for two weeks and divided in to four groups: normal group, WIRS group, WIRS+MOO1 group (treated with MOO at the dose of 1 mL/kg BW), and WIRS+MOO2 group (treated with MOO 2 mL/kg BW). The MOO treatment was given orally for 23 days. On day 24, we checked the behavior parameters, the plasma level of cortisol, acetylcholinesterase (AChE) activity in hippocampus, mRNA expression level of brain-derived neurotrophic factor (BDNF) and oxidative stress parameters in brain tissues. In addition, we also checked the histopathological features of the gastric mucosa wall. Administration of MOO ameliorated anxiety-like, depression-like and memory impairment phenotypes in the WIRS mouse model although the plasma cortisol concentrations were comparable among the groups. Of note, MOO both in two doses could suppress the AChE activity in hippocampus tissue and ameliorated the MDA level in prefrontal cortex tissue in mice exposed to WIRS. Although only WIRS+MOO2 group could increase the mRNA expression of BDNF, the histopathological gastric mucosa wall features were improved in all MOO groups. Taken together, these finding suggested that MOO may have a neuroprotective effect in the mouse model of WIRS as evidenced by improving the abnormal behaviors through enhancing mRNA expression level of BDNF, inhibited AChE activity, and prevented the increase of MDA level in the brain.

Taurine attenuated methotrexate-induced intestinal injury by regulating NF-κB/iNOS and Keap1/Nrf2/HO-1 signals

Methotrexate (MTX) is a well-known and widely used cytotoxic chemotherapeutic agent. However, intestinal mucosa damage is a serious adverse effect of MTX. Taurine (TUR) is a sulfur-containing free β-amino acid with antioxidant and therapeutic value against several diseases. The current study aimed to determine the protective effect of TUR against MTX-induced intestinal injury. Rats were allocated into four groups. The first group received vehicles only. The second group received TUR at a dose of 250 mg/kg i.p. For induction of intestinal injury, the rats in the third group were given MTX once at a dose of 20 mg/kg, i.p. The fourth group received TUR 7 days before and 7 days after MTX, as previously described. TUR significantly attenuated the cytokine release by suppressing NF-κB and iNOS expressions. Moreover, cotreatment with TUR attenuated the increased MDA level while it enhanced the antioxidant GSH and SOD levels mediated by effective downregulation of Keap1 expression, while the expression of Nrf2, HO-1, and cytoglobin were up-regulated. Additionally, TUR mitigated the apoptosis and proliferation indices by decreasing the elevated levels of intestinal PCNA and caspase-3. Finally, TUR potently increased the cytotoxic activity of MTX toward Caco-2, MCF-7, and A549 cancer cells. In conclusion, TUR was a promising agent for relieving MTX-mediated intestinal injury via various antioxidant, anti-inflammatory, and antiapoptotic mechanisms.

Curcumin-loaded cockle shell-derived calcium carbonate nanoparticles ameliorates lead-induced neurotoxicity in rats via attenuation of oxidative stress.

A substantial global health burden is associated with neurotoxicity caused by lead (Pb) exposure and the common mechanism of this toxicity is mainly via oxidative damage. Curcumin has remarkable pharmacological activities but remains clinically constrained due to its poor bioavailability when orally administered. Currently, cockle shell-derived calcium carbonate nanoparticle (CSCaCO3NP) is gaining more acceptance in nanomedicine as a nanocarrier to various therapeutics. This study aimed at investigating the ameliorative effect of curcumin-loaded CSCaCO3NP (Cur-CSCaCO3NP) on lead-induced neurotoxicity in rats. A total of 36 male Sprague-Dawley rats were randomly assigned into five groups. Each group consists of 6 rats apart from the control group which consists of 12 rats. During the 4 weeks induction phase, all rats received a flat dose of 50 mg/kg of lead while the control group received normal saline. The treatment phase lasted for 4 weeks, and all rats received various doses of treatments as follows: group C (Cur 100) received 100 mg/kg of curcumin, group D (Cur-CSCaCO3NP 50) received 50 mg/kg of Cur-CSCaCO3NP, and group E (Cur-CSCaCO3NP 100) received 100 mg/kg of Cur-CSCaCO3NP. The motor function test was carried out using the horizontal bar method. The cerebral and cerebellar oxidative biomarker levels were estimated using ELISA and enzyme assay kits. Lead-administered rats revealed a significant decrease in motor scores and SOD activities with a resultant increase in MDA levels. Furthermore, marked cellular death of the cerebral and cerebellar cortex was observed. Conversely, treatment with Cur-CSCaCO3NP demonstrated enhanced ameliorative effects when compared with free curcumin treatment by significantly reversing the aforementioned alterations caused by lead. Thus, CSCaCO3NP enhanced the efficacy of curcumin by ameliorating the lead-induced neurotoxicity via enhanced attenuation of oxidative stress.

Effects of Zanthoxylum acanthopodium on MMP-9 and GLUT-1 expression and histology changes in rats with cervical carcinoma

Cervical cancer is one of the most common cancers in Indonesia. It can be treated with molecular therapies targeting Matrix metallopeptidase 9 (MMP-9) and Glucose transporter (GLUT-1), which are enzymes that are involved in tumour cell invasion, metastasis and angiogenesis. Zanthoxylum acanthopodium (andaliman) is an Indonesian herb with anti-cancer properties. This study aimed to investigate the histological changes andaliman treatment caused in MMP-9 and GLUT-1 expression. This study used five groups of rats: control (C-), cancer model (C+), cancer-bearing rats with a 100-mg dose of Zanthoxylum acanthopodium methanol extract (ZAM)/BW (ZAM100), cancer-bearing rats with a 200-mg dose of ZAM /BW (ZAM200) and cancer-bearing rats with a 400-mg dose of ZAM/BW (ZAM400). Immunohistochemical methods were used to stain cervical tissue with MMP-9 and GLUT-1 antibodies, and a TUNEL assay was performed to investigate cell apoptosis. Zanthoxylum acanthopodium methanol extract administration did not affect rat body weight but had a significant effect on cervical cancer growth. There was an increase in MDA levels associated with SOD deficiency in tumour tissue. SOD activity increased due to ZAM administration, allowing cells to be protected from oxidant disruption and oxidative stress. ZAM ameliorated cervical carcinoma tissue damage and reduced the expression of MMP-9, GLUT-1 and apoptosis in serum and tissue (p &amp;lt; 0.01) In short, the higher the ZAM dose, the lower the expression of MMP-9, GLUT-1 and apoptosis, indicating that ZAM is effective to treat cervical cancer.

17β-Estradiol Inhibits Oxidative Damage in Cataracts Rats via NOTCH1 Signaling

This study assesses the effect of 17β-estradiol on oxidative damage and NOTCH1 levels in cataract rats. 45 SD rats, aged 8–12 weeks old and weighted 225–312 g were assigned into healthy group, cataract group, and treatment group with n = 15 in each group followed by analysis of the pathological morphology of rat lens by HE staining, cell apoptosis by flow cytometry, and the degree of turbidity under a microscope. Meanwhile, MDA and SOD levels were measured and NOTCH1, p53 and BAX expressions was detected by PT-PCR. The Healthy group rats showed complete and orderly lens structure, whereas, the cataract group showed disorganized and distributed loosely lens, with the formation of vacuoles and the rupture and degradation of fibrocells. In the treatment group, the lens epithelial cells were orderly and evenly distributed, and the vacuoles were significantly reduced. The apoptotic rate of lens epithelial cells in healthy group (1.79±0.11)% was significantly lower than that in cataract group (15.22±1.17)% (P &lt; 0.05), which showed significantly higher apoptotic rate than treatment group (6.31±1.12)% (P &lt; 0.05). The degree of eye turbidity was increased in cataract group and reduced in treatment group compared with that in healthy group (P &lt; 0.05). In addition, cataract group showed significantly reduced SOD and increased MDA level groups along with upregulated Notch1, p53 and Bax (P &lt; 0.05). However, treatment group showed significantly increased SOD, decreased MDA and downregulated Notch1, p53 and Bax. In conclusion, 17β-estradiol reduces the apoptosis rate of lens epithelial cells in cataract rats by reducing NOTCH1 level, thereby enhancing the ability to resist oxidative damage.

L-carnitine Prevents Hepatic Steatosis in Deep-Frying Oil-Treated Rat

Deep-frying oil is a source of free radicals that causes oxidative stress in the body and lead to chronic and degenerative diseases, including non-alcoholic fatty liver (NAFLD). Steatosis, or fatty liver, is one of NAFLD and is a common result of moderate to severe hepatocellular insult. L-Carnitine involves in the metabolism of fat and has a potential role as an antioxidant. In the present study, we aimed to elucidate the role of L-Carnitine in deep-frying oil-treated rats. We equally divided thirty-six male Wistar albino rats into three groups: the group of rats without any treatment (control group), the group of rats treated with deep-frying oil of 0.42 ml/rat/day (negative control group), and the group of rats co-treated with deep-frying oil of 0.42 ml/rat/day and L-Carnitine of 30 mg/kg/day (treatment group). After three weeks of experimental treatment, we found that the deep-frying oil treatment in negative control group caused a significant elevation in the number of hepatic steatosis, hepatic TG content and serum ALT and AST accompanied by increased MDA levels, suggesting the oxidative stress-induced fatty liver. The treatment of L-Carnitine reduced the number of hepatic steatosis and TG content, as well as serum ALT and AST levels. To test the involvement of antioxidant activity of L-Carnitine to its beneficial effects on the development of fatty liver, we observed the expression of endogenous antioxidant. We found that the expression of hepatic SOD, CAT, and GPx were up-regulated by L-Carnitine, followed by a concomitant depletion of MDA levels. In general, this study suggests that L-Carnitine prevents the development of hepatic steatosis and oxidative damage, as well as improves the hepatic antioxidant defenses.

Neuroprotective effect of anethole against rotenone induced non-motor deficits and oxidative stress in rat model of Parkinson’s disease

IntroductionNon-motor symptoms (NMS) have high prevalence in patients with Parkinson’s disease (PD). These symptoms are mainly the result of increased oxidative stress and neuronal damage. In this study we investigated the possible neuroprotective effects of anethole as a potent antioxidant on rotenone-induced behavioral deficits, hippocampal neuronal death, and oxidative stress profile in rats. MethodsMale Wistar rats were administered with anethole (62.5, 125, and 250 mg/kg, i.g) concomitantly with rotenone (2 mg/kg, s.c) for 35 days. Shuttle box and novel object recognition tests were performed to determine cognitive functions, and tail flick test was used to measure pain sensitivity. The levels of BDNF, MDA, SOD, and GPx were assayed in the hippocampus. Hippocampal neuronal damage was evaluated using cresyl violet staining technique. ResultsChronic administration of rotenone induced cognitive deficit and reduced thermal pain threshold. Rotenone also decreased SOD and GPx activities, increased MDA level, and reduced the expression of BDNF in the hippocampus. In addition, hippocampal neuronal loss was increased in rotenone treated rats. Treatment with high dose of anethole (250 mg/kg) improved cognitive function and increased pain threshold in all three doses (62.5, 125, and 250 mg/kg). Despite the unchanged SOD and GPx activities, hippocampal levels of MDA was significantly decreased after high-dose anethole treatment. Moreover, High dose of anethole increased the number of surviving neurons in the hippocampus, but couldn’t increase the BDNF expression. ConclusionOur findings indicated that anethole has antioxidant and neuroprotective effects against non-motor disorders induced by rotenone toxicity.

Impact of melatonin on the hydrogen peroxide treatment efficacy in Microcystis aeruginosa: Cell growth, oxidative stress response, and gene transcription

A study was conducted to determine how melatonin (MLT), a growth regulator, affects Microcystis aeruginosa cell behaviour and how MLT exposed cells respond to hydrogen peroxide (H2O2) treatment. MLT promotes the growth, chl-a content, Fv/Fm values, and microcystins (MCs) production of M. aeruginosa at low concentrations of 1–2.5 μmol/L but suppresses the growth at high concentrations (5–10 μmol/L). The cellular and genetic responses of MLT pre-treated cells to H2O2 treatment were examined further. Further research found that the cells pre-treated with MLT were susceptible to a range of growth-promoting, inhibiting and lethal effects when exposed to higher levels of H2O2. A dose-dependent pattern was observed under conditions of 0.05–0.2 mmol/L H2O2 with 0.5–2.5 μmol/L MLT concentrations to different degrees. High doses of H2O2 (0.2 and 0.3 mmol/L) typically lead to cell lysis and release of MCs in 5.0 and 10 μmol/L MLT pre-treated cells. A decrease in SOD/CAT activities and an increase in MDA levels validated the growth reduction. Furthermore, higher cell lysis and release of intracellular MCs were observed when H2O2 was increased for 5–10 μmol/L MLT pre-treated cells. This led to a higher accumulation of extracellular MCs. The results provide insight into how MLT influences H2O2 damage and assist in identifying situations where H2O2 treatment of cyanobacterial blooms is most appropriate.