Tissue Malondialdehyde Levels Research Articles

Resolvin D1 alleviates cerebral ischemia/reperfusion injury in rats by inhibiting NLRP3 signaling pathway.

The purpose of the present study was to investigate the role of resolvin D1 (RvD1) in cerebral ischemia/ reperfusion (I/R) injury in rats and its mechanism. A total of 60 adult male Wistar rats were divided into 3 groups using a random number table, including sham-operation group (Sham group, n=20), cerebral I/R injury group (I/R group, n=20) and cerebral I/R injury + RvD1 pretreatment group (I/R + RvD1 group, n=20). The model of focal I/R injury was established using suture method through 30 min of ischemia and 24 h of reperfusion. In I/R + RvD1 group, the rats were intraperitoneally injected with RvD1 (4 mg/kg/d) at 7 d before operation, while those in the Sham group and I/R group were injected with an equal volume of normal saline. After reperfusion, the area of cerebral infarction was evaluated by means of 2,3,5-triphenyltetrazolium chloride (TTC) staining. Then hematoxylin and eosin (H&E) staining was applied to observe the status of brain tissue injury in each group of rats, and the expression of malondialdehyde (MDA), a marker of oxidative stress, in each group of brain tissues was detected via an oxidative stress detection kit. Moreover, reverse transcription-polymerase chain reaction (RT-PCR) assay was performed to measure the levels of inflammation-related genes [interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α)] in the brain tissues of each group of rats, and the neuronal apoptosis level in the brain tissues in each group was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Finally, the expression levels of proteins related to the inflammasome signaling pathway were detected via Western blotting assay. It was indicated in the results of TTC staining and H&E staining that RvD1 could remarkably decrease the area of I/R-induced cerebral infarction and relieve nervous tissue injury (P<0.05). The results of TUNEL staining revealed that the cerebral neuronal apoptosis induced by I/R injury was alleviated by RvD1 (P<0.05). In addition, RvD1 lowered the levels of inflammatory factors and MDA in the brain tissues of rats with I/R injury (P<0.05). Furthermore, it was discovered that RvD1 repressed the protein expression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) in the brain tissues of rats with I/R injury (P<0.05). The protective effect of RvD1 on the rats against cerebral I/R injury may be related to its inhibition on NLRP3 inflammasome, and RvD1 is expected to become a targeted drug for the clinical treatment of cerebral I/R injury.

Profound Hypotension before Aortic Clamping Can Exacerbate Spinal Cord Ischemic Injury after Aortic Surgery in Rats.

Spinal cord ischemia is one of the most serious complications of aortic repair in patients with acute aortic syndrome. However, the effect of hypotension before aortic clamping on spinal cord injury has not been documented. A total of 48 male Sprague-Dawley rats were randomly divided into four groups: the sham group; control group (mean arterial pressure (MAP) < 90% of baseline value before aortic clamping); mild hypotension group (MAP < 80%); and profound hypotension group (MAP < 60%). Spinal cord ischemia was induced using a balloon-tipped catheter placed in the descending thoracic aorta. Neurological function of the hind limbs was evaluated for seven days after reperfusion and recorded using a motor deficit index (MDI). The spinal cord was then harvested for histopathological examination and evaluation of oxidative stress and inflammation. The profound hypotension group demonstrated a significantly higher MDI 48 h post-reperfusion and lower number of normal motor neurons than the other groups (p < 0.001). The levels of tissue malondialdehyde and tumor necrosis factor-α (TNF-α) were also significantly increased in the profound hypotension group compared with other groups. Profound hypotension before aortic clamping can aggravate neurologic outcomes after aortic surgery by exacerbating neurologic injury and reducing the number of normal motor neurons.

Phytotoxicity, Morphological, and Metabolic Effects of the Sesquiterpenoid Nerolidol on Arabidopsis thaliana Seedling Roots.

Natural herbicides that are based on allelopathy of compounds, can offer effective alternatives to chemical herbicides towards sustainable agricultural practices. Nerolidol, a sesquiterpenoid alcohol synthesized by many plant families, was shown to be the most effective allelopathic compound in a preliminary screening performed with several other sesquiterpenoids. In the present study, Arabidopsis thaliana seedlings were treated for 14 d with various cis-nerolidol concentrations (0, 50, 100, 200, 400, and 800 µM) to investigate its effects on root growth and morphology. To probe the underlying changes in root metabolome, we conducted untargeted gas chromatography mass spectrometry (GC-MS) based metabolomics to find out the specificity or multi-target action of this sesquiterpenoid alcohol. Oxidative stress (measured as levels of H2O2 and malondialdehyde (MDA) by-product) and antioxidant enzyme activities, i.e., superoxide dismutase (SOD) and catalase (CAT) were also evaluated in the roots. Nerolidol showed an IC50 (120 µM), which can be considered low for natural products. Nerolidol caused alterations in root morphology, brought changes in auxin balance, induced changes in sugar, amino acid, and carboxylic acid profiles, and increased the levels of H2O2 and MDA in root tissues in a dose-dependent manner. Several metabolomic-scale changes induced by nerolidol support the multi-target action of nerolidol, which is a positive feature for a botanical herbicide. Though it warrants further mechanistic investigation, nerolidol is a promising compound for developing a new natural herbicide.

Streptozotosin ile İndüklenmiş Diyabetik Sıçanlarda Melatoninin Antioksidan Aktivitesi; Kan ve Karaciğer Dokusunda

OBJECTIVE: In this study, it was aimed to investigate the antioxidant protective effect of melatonin supplementation against oxidative damage in blood and liver tissues of rats with experimental type 1 diabetes with Streptozotocin (STZ). MATERIALS AND METHODS: Forty adult Spraque Dawley male rats; Group 1-Control group, Group 2-diabetes group, Group 3- melatonin supplement group and Group 4- diabetes and melatonin supplement group were divided into four groups. Diabetes was induced in rats by administering a single dose of 60 mg / kg STZ intraperitoneally. Melatonin supplementation was administered at a dose of 10 mg / kg / day subcutaneously for 6 weeks. Glutathione (GSH), catalase (CAT) and malondialdehyde (MDA) levels were measured spectrophotometrically in the liver and serum samples taken at the end of the experiment. RESULTS: The results of the study showed that MDA levels increased in the serum and liver tissues of diabetic animals. It was observed that melatonin administration decreased MDA levels in both tissues, increased GSH and CAT levels or kept them stable by preventing it from falling (p <0.05). CONCLUSION: The results of this study are consistent with the consensus that emphasizes and accepts that one of the main causes of complications of diabetes is oxidative stress. Our results show that melatonin has an ameliorating effect on increased oxidative stress in diabetes and melatonin can be used as a therapeutic agent.

Protective Effect of Sodium Selenite on 4-Nonylphenol-Induced Hepatotoxicity and Nephrotoxicity in Rats.

This study was aimed at evaluating the protective effect of sodium selenite (SS) on DNA integrity, antioxidant/oxidant status, and histological changes on 4-nonylphenol (4-NP)-induced toxicity in liver and kidney tissues of rats. Twenty-four adult male Sprague Dawley rats were divided into 4 groups as control, SS, 4-NP, and SS+4-NP group. Control group was untreated. The SS group was supplemented with SS (0.5mg/kg/day) and the 4-NP group was given 4-NP (125mg/kg/day). The rats in the SS+4-NP group received SS followed by 4-NP 1h later at the abovementioned doses. The treatments were administered by oral gavage for 48days. DNA damage was analyzed by comet assay in lymphocytes. Oxidative stress parameters were measured, and histological evaluation was performed in liver and kidney tissues. Results showed that SS administration significantly decreased % Tail DNA and Mean Tail Moment in SS+4-NP group as compared with 4-NP group. Catalase activity in liver was significantly lower in 4-NP group only. SS treatment significantly increased the glutathione level and decreased high malondialdehyde level in tissues of the SS+4-NP group as compared with 4-NP group. Dilation of central vein, ballooning degeneration, vacuolar degeneration, and deterioration in the structure of remark cords in 4-NP-administered were alleviated in rats that received SS supplementation before administration of 4-NP. Moreover, glycogen intensity in hepatocytes and the wall of central vein increased in the SS+4-NP group. In addition, the SS supplementation in the SS+4-NP group decreased glomerular degeneration as well as the width of cavum glomeruli and congestion intensity in the kidney. These results indicate that SS may have a protective effect against 4-NP-induced hepato-nephrotoxicity in rats.

Does Ginger Protect Against Ovarian Damage in Rats Induced by Sodium Metabisulfite Toxicity? An Experimental Evidence

Background: Sulfites including Sodium Metabisulfite (SMB) are commonly used as food preservatives and pharmaceutical products. Despite their worldwide use, there is evidence suggesting their toxicity on human organs and tissues. The purpose of this study was to evaluate the effect of SMB with or without Zingiber officinale (ginger) extract on the rat ovary. Methods: A total of 32 adult, female Wistar rats were divided into four groups of eight each. They consisted of, a) control group, b) ginger group (500 mg/kg/day), c) SMB group (260 mg/kg/day), and d) combined SMB and ginger group at identical doses. After 28 days, the rats were sacrificed and the ovarian tissue Malondialdehyde (MDA), as a marker of lipid peroxidation was measured. The volume and weight of the ovaries and the number of follicles at different stages were counted by stereological methods. Results: The SMB treatment caused a significant decrease in the ovarian volume and the number of follicles with simultaneous increase in the number of degenerate follicles (P≤0.001) and MDA level (P≤0.01). Ginger treatment of the rats exposed to SMB significantly increased the number of follicles at various stages and partially reversed the ovarian tissue level of MDA, compared to that in the control group (P≤0.05). Conclusion: The SMB treatment induced structural changes in the rats’ ovaries and the concomitant treatment with ginger largely reversed the damages caused by SMB.

Effects of the fermentedZizyphus jujubain the amyloid β25-35-induced Alzheimer's disease mouse model

BACKGROUD/OBJECTIVESAlzheimer's disease (AD) is the most common cause of dementia in the elderly. Due to the increased incidence of dementia, there is a corresponding increase concerning the importance of AD. In this study, we investigated the protective effects conferred by Zizyphus jujuba (Zj) and Zizyphus jujuba fermented by yeast (Zj-Y), on cognitive impairment in an AD mouse model.MATERIALS/METHODSAD was induced by injecting amyloid beta25-35 (Aβ25-35) in ICR mice, and subsequently 200 mg/kg Zj or Zj-Y was administered daily for 14 days. The cognitive ability of AD mice was observed through behavioral experiments in T-maze, novel object recognition, and Morris water maze tests. We subsequently measured the levels of malondialdehyde (MDA), nitric oxide (NO), aspartate aminotransferase, and alanine aminotransferase in either tissues or serum.RESULTSIn behavioral tests, deterioration was revealed in the short- and long-term learning and memory functions in the Aβ25-35-injected control group compared to the normal group, indicating that Aβ25-35 injection impairs cognitive functions. However, administration of Zj and Zj-Y improved cognitive function in mice, as compared to the Aβ25-35-injected control mice. In addition, the Aβ25-35 induced elevations of MDA and NO in the brain, kidney, and liver were suppressed after exposure to Zj and Zj-Y. Especially, Zj-Y showed stronger scavenging effect against MDA and NO, as compared to Zj.CONCLUSIONSResults of the present study indicate that Zj-Y exerts a protective effect on cognitive impairment and memory dysfunction, which is exerted by attenuating the oxidative stress induced by Aβ25-35.

Protective effects of nebivolol on ovarian ischemia-reperfusion injury in rat.

Ovarian torsion is a common gynecological emergency of reproductive ages, occurring at rates of 2.7-7.4%. This study aimed to evaluate the antioxidant effects of Nebivolol (NEB) and histopathological changes in experimental ischemic (I) and ischemic-reperfusion (I/R) injury in rat ovaries. Forty-eight adult female rats were randomly separated into six groups as group 1 (control) receiving an oral saline solution for 3 days; group 2 (I) that underwent ischemia for 3 h with the application of atraumatic vascular clips; group 3 (I/R); group 4 (I + NEB) receiving 10 mg/kg NEB by oral gavage 30 min prior to the ischemia induction; group 5 (I/R + NEB) receiving 10 mg/kg NEB, and group 6 (control + NEB) receiving oral 10 mg/kg NEB for 3 days before ischemia induction followed by consequent reperfusion. Ovarian tissue damage was scored by histopathological analysis. Ovarian tissue malondialdehyde (MDA) and glutathione (GSH) levels were measured biochemically. The levels of MDA and tumor necrosis factor-alpha (TNF-α), and TUNEL assay positivity scores increased in the I and I/R groups. GSH levels decreased in all case groups (P < 0.05). The oral administration of NEB (10 mg/kg) to the I- and I/R-groups reduced the levels of MDA and TNF-α and TUNEL assay immunopositivity scores (P < 0.05). GSH levels increased in the treatment groups. The current experimental ovarian torsion study suggests a protective role for NEB against I and I/R injury in rat ovaries. NEB may be a novel agent for decreasing ovarian I/R injury.

Ameliorating and protective effects mesalazine on ethanol-induced gastric ulcers in experimental rats

Gastric ulcer is a frequent gastrointestinal tract (GIT) disorder that affects about 10% of the world population. Drug candidates that can provide high efficacy and low toxicity are needed value for the prevention and treatment of gastric ulcers. The present study aimed to assess the protective effect of mesalazine against ethanol-induced gastric mucosal injury in rats. The rats were divided into five groups, normal, ethanolic, standard (recipient ranitidine 50 mg/kg), experimental groups 1, 2 (receive mesalazine at doses of 50 and 100, respectively). The protective effect of mesalazine was evaluated by the ulcer index, histological examinations, measurement of oxidative stress parameters, antioxidant systems, and some gastric mucosal protection factors.Pre-treatment of rats with doses of 50 and 100 mg/kg Mesalazine (5-ASA) in experimental groups 1 and 2 increased the pH of gastric juice and reduced the gastric ulcer index compared to the ethanolic group. Also, the results indicated that mesalazine, reduced the tissue reactive oxygen species (ROS), malondialdehyde (MDA), and protein carbonyl (PCO) levels, serum nitric oxide (NO), and increased the level of tissue NO and glutathione (GSH) and activity of Catalase (CAT), Based on these results, it can be concluded that mesalazine strengthens the antioxidant defense system of gastric mucosal cells during oxidative damage caused by ethanol.

The effect of a natural molecule in ovary ischemia reperfusion damage: does lycopene protect ovary?

Ovarian ischemia is a gynecological emergency case that occurs as a result of ovarian torsion. Oxidative stress plays a central role in the development of ischemia/reperfusion (IR) injuries. Lycopene (LYC) is a lipophilic, natural carotenoid well known for its antioxidant properties. This study provides information on the potential applications of lycopene. The Wistar Albino rats were distributed into six groups: Sham group (only a laparotomy was performed), Control group [laparotomy and intraperitoneal dissolvent (olive oil)], IR group, IR+olive oil group, IR+LYC 2.5 mg/kg/dose, intraperitoneal group, IR+LYC 5 mg/kg/dose intraperitoneal group. Evaluated in terms of histopathological changes, tissue malondialdehyde levels (MDA), ovarian expressions of phosphorylated nuclear factor-kappa B (p-NF-κB) and the TUNEL method was utilized to show apoptosis of ovarian tissue. There was a significant decrease in MDA, p-NF-κB values and the proportion of apoptotic cells assessed by TUNEL compared to the group that did not receive intraperitoneal LYC in rat injury with IR damage (P<0.05). In histopathological damage scoring, it was observed that the cell damage was significantly reduced in LYC-administered groups. LYC showed significant ameliorative effects on ovary injury caused by IR through acting as an antioxidant, antiinflammatory, and antiapoptotic agent.

Lycopene hampers lung injury due to skeletal muscle ischemia-reperfusion in rat model.

This study investigates lycopene's preventive efficacy in skeletal muscle ischemia-reperfusion (I/R) induced lung injury. Thirty-two rats were randomly assigned to control group, lycopene group, I/R group and I/R+lycopene group. In the lycopene and I/R+lycopene groups, the rats initially received 10mg/kg/day lycopene orally for 15 days. Then, dissection around the abdominal aorta was performed in all rats under general anesthesia. The aorta was clamped at the infrarenal level in the I/R group and I/R+lycopene group for two hours before two hours of reperfusion. The mean serum levels of malondialdehyde (53.0±20.14nmol/mL) and superoxide dismutase (1.03±0.16U/mL) were higher and lower in the I/R group than the other three groups, respectively (p<0.001). The mean serum IMA level of I/R+lycopene group (0.42±0.04 abs/u) was lower than the I/R group (0.47±0.04 abs/u) (p=0.015). The mean tissue malondialdehyde levels of I/R group (69.10±11.55nmol/mL) and I/R+lycopene group (68.36±21.17nmol/mL) were high compared to the control group (49.87±6.52nmol/mL) and lycopene group (47.82±4.44nmol/mL) (p=0.002). The mean tissue glutathione peroxidase (p<0.001) and superoxide dismutase (p=0.001) levels of I/R group (121.81±43.59nmol/mL and 25.17±8.69U/mL) were low compared to the control group (236.12±18.01nmol/mL and 46.30±5.17U/mL), lycopene group (227.52±16.92nmol/mL and 45.82±4.02U/mL), and I/R+lycopene group (176.02±24.27nmol/mL and 35.20±4.85U/mL). The histopathological analyses of I/R+lycopene group indicated less significant changes than the control group. Tissue damage in the I/R+lycopene group was less prominent than the I/R group. These findings suggest oral lycopene supplementation as a promising prevention against skeletal muscle I/R caused lung injury.

Etiology of Liver Steatosis Influences the Severity of Ischemia/Reperfusion Injury and Survival After Liver Transplantation in Rats.

Liver steatosis is a leading cause of graft disposal in liver transplantation, though the degree of steatosis is often the single factor determining acceptability of the graft. We investigated how the cause of liver steatosis affects graft function in rat orthotopic liver transplantation (OLT). OLT was performed using 2 types of steatotic liver grafts: the fasting and hyperalimentation (FHA) model and the methionine- and choline-deficient diet models. The FHA and 4-week feeding of a methionine- and choline-deficient diet (MCDD4wk) groups showed similar liver triglyceride levels without signs of steatohepatitis. Therefore, the 2 groups were compared in the following experiment. With 6-hour cold storage, the 7-day survival rate after OLT was far worse in the FHA than in the MCDD4wk group (0% versus 100%, P=0.002). With 1-hour cold storage, the FHA group showed higher aspartate aminotransferase and alanine aminotransferase levels and histological injury scores in zones 1 and 2 at 24hours after reperfusion than the normal liver and MCDD4wk groups. Intrahepatic microcirculation and tissue adenosine triphosphate levels were significantly lower in the FHA group after reperfusion. Hepatocyte necrosis, sinusoidal endothelial cell injury, and abnormal swelling of the mitochondria were also found in the FHA group after reperfusion. Tissue malondialdehyde levels were higher in the MCDD4wk group before and after reperfusion. However, the grafts up-regulated several antioxidant enzymes soon after reperfusion. Even though the degree of steatosis was equivalent, the 2 liver steatosis models possessed quite unique basal characteristics and showed completely different responses against ischemia/reperfusion injury and survival after transplantation. Our results demonstrate that the degree of fat accumulation is not a single determinant for the usability of steatotic liver grafts.

Effects of myricetin on testicular torsion-detorsion injury in rats.

Testicular torsion is an emergency, and unless there is an urgent intervention, irreversible ischaemic damage and gonad loss occur in the testicle. We aimed to investigate myricetin's antioxidant properties as well as its protective effect against ischaemia-reperfusion (I/R) damage in the testicular torsion model. A total of 18 rats were divided into three equal groups. Group 1 was the sham group. Group 2: testicular torsion was performed, and orchiectomy was done 2hr after detorsion. Group 3: received torsion and 1mg/kg intraperitoneal myricetin was given 30min before detorsion, and orchiectomy was applied 2hr after detorsion. We evaluated tissue malondialdehyde, superoxide dismutase, and catalase levels and Johnsen Testicular Biopsy Score to show its histopathological effect. There was a statistically significant decrease in MDA values in myricetin group compared to Group 2 (p<.017). There was no significant difference in the statistical analysis of SOD and CAT values (p=.337 and p=.025). There was a statistically significant difference in testicular I/R damage in the myricetin group compared to Group 1 and Group 2 (p<.017). Myricetin treatment significantly decreased testicular tissue damage compared to the torsion group but did not reach the values close to the control group.

The effect of Myrtus communis L. ethanol extract on the small intestine and lungs in experimental thermal burn injury.

Thermal trauma can damage organs away from the skin burn site and lead to multiple organ dysfunction. Following thermal injury, all tissues are exposed to ischemia, and as a result, resuscitation and reperfusion occur during the burning shock. Burn damage starts systemic inflammatory reactions that produce toxins and reactive oxygen radicals that lead to peroxidation. This study aimed to investigate, for the first time, the possible antioxidant effects of Myrtus communis ethanol extract on burn-induced oxidative distant organ injury orally. The thermal trauma was generated under ether anesthesia by exposing the dorsum of rats to 90°C water bath for 10s. 100mg/kg/day Mrytus communis ethanol extract was applied orally for two days. Malondialdehyde (MDA) and glutathione (GSH) levels, glutatinone-S-transferase (GST), superoxidedismutase (SOD) and catalase (CAT) activities were determined to detect the possible antioxidant effects of myrtle on small intestine and lung tissues. Burn damage significantly increased MDA levels in lung and small intestine tissues, and significantly decreased GSH levels, CAT and GST activities in the small intestine and lung tissues compared to control group. Mrytus communis ethanol extract decreased MDA level and increased GSH level, SOD, CAT and GST activities significantly in either small intestine or lung tissues. Mrytus communis extract may be an ideal candidate to be used as an antioxidant adjunct to improve oxidative distant organ damage to limit the systemic inflammatory response and decreasing the recovery time after thermal injury.

Characterisation and Hypolipidaemic Activity of Phenylquinoline, and Narceine Isolated from Ficus polita Leaf

Aim: To evaluate hypolipidaemic potentials of column chromatography fractions (F1 to F6) of the chloroform leaf extract of Ficus polita and to detect the bioactive compounds present in the most active fraction using spectroscopic techniques.&#x0D; Study Design: Fourty-five (45) wistar rats were grouped into nine groups of five rats each: normal control, hyperlipidaemic control, hyperlipidaemic administered with standard drug control/ atorvastatin (10 mg/kg body weight), and hyperlipidaemic administered groups administered with 50 mg/kg body weight of column chromatography fractions (F1, F2, F3, F4, F5, and F6) for a period of two weeks.&#x0D; Place and Duration of Study: Department of Biochemistry Laboratory, Faculty of Basic Medical Sciences, Bayero University Kano, Nigeria, from May 2018 to April 2019.&#x0D; Methodology: Chloroform leaf extract of F. polita was fractionated by using column chromatography, and the resulting fractions were pooled, based on their retention factor (Rf), into six (6) fractions by using analytical thin layer chromatography. The resulting six (6) fractions were screened for hypolipidaemic activity. Serum total cholesterol (TC), triglycerides (TG), high density lipoprotein-cholesterol (HDL), and low density lipoprotein cholesterol (LDL) were determined. The rats treated with the best fraction in terms hypolipidaemic activity (fraction 3) were screened for serum HMG Co A reductase, lactate dehydrogenase (LDH), creatine kinase (CK) activities, as well as troponin I level. Oxidative stress markers such as malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were determined in the heart tissue homogenate of the rats treated with fraction 3.&#x0D; Results: Fraction 3 treated hyperlipidaemic group showed significant (p&lt;0.05) decrease in the levels of serum TC, TG, and LDL, but significant (p&lt;0.05) increase in the level of serum HDL. Fraction 3 (F3) treated hyperlipidaemic groups showed significant (p&lt;0.05) decrease in the activity of serum LDH and the level of troponin I, but significant (p&lt;0.05) increase in the activity of serum HMG Co A reductase. After high fat diet administration, the level of heart tissue antioxidant markers such as GSH, SOD and catalase were decreased whereas the level of heart tissue MDA was elevated. The level of these antioxidant markers were brought to normalcy by fraction 3 (F3). Histological studies of the heart corroborated the biochemical findings, and treatment with fraction 3 (F3) was found to be effective in restoring dietary-induced myocardiac toxicity in rats. FTIR and GCMS analyses were carried out for the detection of bioactive compound(s) in fraction 3 (F3), and the result revealed the presence of "8-methoxy-4-phenylquinoline, and narceine.&#x0D; Conclusion: The study concludes that; the hypolipidaemic property of the leaf of F. polita is mediated by the bioactive compounds "8-methoxy-4-phenylquinoline, and narceine." via their antioxidant properties.

Investigation of the effects of tadalafil and telmisartan in bleomycin-induced pulmonary fibrosis on rats

Aim: Pulmonary toxicity related to bleomycin, an antitumor drug used in the treatment of several malignancies, is a challenge, and studies to find out molecules to prevent it are ongoing. In this study, we aimed to investigate the effectiveness of telmisartan and tadalafil in an experimental rat model of bleomycin-induced lung fibrosis. Methods: A total of 32 male rats were divided into four groups: Control group, Bleomycin group, Bleomycin-plus-Tadalafil group and Bleomycin-plus-Telmisartan group. Lung fibrosis was achieved by intratracheal administration of bleomycin, and the same procedure was performed to the control group, but saline was substituted for bleomycin. Tadalafil and telmisartan were administered with an orogastric catheter for 14 days. Tissue malondialdehyde levels (MDA) were determined using colorimetric methods. Masson’s trichrome staining was used in the histological examination of the tissue samples. Results: The fibrosis scores of bleomycin-plus-tadalafil and bleomycin-plus-telmisartan groups were lower than that of the bleomycin group (P=0.007 and P=0.007, respectively). MDA levels did not differ among study groups. Conclusion: Tadalafil and telmisartan were found to decrease fibrosis scores, which were increased with bleomycin, concluding that pulmonary toxicity was related to multiple processes and preventable.

Chemo-Protective Potential of Cerium Oxide Nanoparticles against Fipronil-Induced Oxidative Stress, Apoptosis, Inflammation and Reproductive Dysfunction in Male White Albino Rats.

Fipronil (FIP) is an insecticide commonly used in many fields, such as agriculture, veterinary medicine, and public health, and recently it has been proposed as a potential endocrine disrupter. The purpose of this study was to inspect the reproductive impacts of FIP and the possible protective effects of cerium nanoparticles (CeNPs) on male albino rats. Rats received FIP (5 mg/kg bwt; 1/20 LD50), CeNPs (35 mg/kg bwt) and FIP+CeNPs per os daily for 28 days. Serum testosterone levels, testicular oxidative damage, histopathological and immunohistochemical changes were evaluated. FIP provoked testicular oxidative damage as indicated by decreased serum testosterone (≈60%) and superoxide dismutase (≈50%), glutathione peroxidase activity (≈46.67%) and increased malondialdehyde (≈116.67%) and nitric oxide (≈87.5%) levels in testicular tissues. Furthermore, FIP induced edematous changes and degeneration within the seminiferous tubules, hyperplasia, vacuolations, and apoptosis in the epididymides. In addition, FIP exposure upregulated interleukin-1β (IL-1β), nitric oxide synthase 2 (NOS), caspase-3 (Casp3) and downregulated the Burkitt-cell lymphomas (BCL-2), inhibin B proteins (IBP), and androgen receptor (Ar) mRNA expressions Casp3, nitric oxide synthase (iNOS), ionized calcium-binding adapter molecule 1(IBA1), and IL-1β immunoreactions were increased. Also, reduction of proliferating cell nuclear antigen (PCNA), mouse vasa homologue (MVH), and SOX9 protein reactions were reported. Interestingly, CeNPs diminished the harmful impacts of FIP on testicular tissue by decreasing lipid peroxidation, apoptosis and inflammation and increasing the antioxidant activities. The findings reported herein showed that the CeNPs might serve as a supposedly new and efficient protective agent toward reproductive toxicity caused by the FIP insecticide in white male rats.

Chitosan protects liver against ischemia-reperfusion injury via regulating Bcl-2/Bax, TNF-α and TGF-β expression

The study aimed to investigate the potential attenuation effect of chitosan in liver ischemia/reperfusion injury (I/R), and its relevant protective mechanisms. Chitosan (200 mg/kg) has been administered orally for 30 days, later animals underwent liver 45 min ischemia and reperfusion for 60 min. Following treatment with chitosan, the levels of serum aminotransferases and lactate dehydrogenase were significantly reduced. Similarly, hepatic (GSH, SOD, CAT, GST and GPx) were enhanced, and the level of tissue malondialdehyde (MDA) was decreased. In addition, inflammatory cytokinesis (TNF-α and TGF-β) have recorded a significant decrease in their mRNA expression and protein levels using qPCR and ELISA respectively. Marked reduction of apoptosis has been indicated by the elevation in BCL2, and decreasing in BAX, Caspace-3 and Cytochrome-c expression levels, which furthermore confirmed by DNA fragmentation assay. The enhancement of the previous parameters resulted in a marked improvement in the liver architectures after chitosan administration. In conclusion, chitosan has proved its efficiency as an anti-inflammatory and antioxidant agent through its inhibitory effect of cytokines and reducing ROS respectively. In addition, chitosan could modulate the changes in histological structure and alleviate apoptosis induced by liver I/R, which recommend it as an efficient agent for protection against liver I/R injury.

Administration of Nicotine Exacerbates the Quinine-induced Structural and Functional Alterations of Testicular Tissue in Adult Rats: An Experimental Study.

In this study the role of nicotine (NCT) administration on the intensity of rat testicular tissue alterations induced by quinine (QU) was evaluated. Forty adult Wistar rats were divided into four groups. Control (CON), NCT administrated (4 mg/kg) (NCT), QU treated (25 mg/kg for 7 days) (QU), and nicotine with quinine received (NCT+QU). After 28 days, serum testosterone and malondialdehyde (MDA) levels were measured. Testes and epididymides samples were prepared for determining tissue MDA levels, histomorphometry, microscopic indices of spermatogenesis, immunohistochemistry of p53 and sperm analysis. Testosterone levels were decreased significantly (P = .0004) in treated groups compared to CON group. Serum MDA levels were increased significantly (P = .0004) in NCT and QU groups compared to CON group. Tissue MDA levels were increased significantly (P = .0012) in NCT+QU group in comparison to CON group. These parameters were changed significantly in NCT+QU group compared to QU group. Seminiferous tubules diameter decreased significantly (P < .0001) in treated groups compared to CON group and in NCT+QU group compared to QU group. The height of germinal epithelium decreased significantly (P = .0001) in NCT and NCT+QU groups compared to CON and QU groups. The number of Sertoli cells, spermatocytes, and spermatids decreased significantly in treated groups compared to CON group. The number of spermatogonia decreased significantly (P = .0017) in NCT and NCT+QU groups compared to CON group. The number of Sertoli cells, spermatogonia, and spermatocytes decreased significantly in NCT+QU group compared to QU group. All indices of spermatogenesis decreased in treated groups compared to CON group. The lowest mean of these indices was observed in NCT+QU group. The sperm viability decreased significantly (P < .0001) in treated groups compared to CON group. Sperm count and motility decreased significantly in NCT and NCT+QU groups compared to CON group. All experimental groups showed the over-expression of p53 compared to CON group. The administration of nicotine could be involved in the exacerbation of testicular tissue alterations related to quinine therapy.

Ceftriaxone improves hepatorenal damages in mice subjected to D-galactose-induced aging

Ceftriaxone (CTX) is a third-generation cephalosporin antibiotic that has broad-spectrum antimicrobial activity. This agent also has anti-inflammatory and antioxidant characteristics. In the current study, the effects of CTX against hepatorenal damages in a D-galactose (DGL) induced aging model were investigated. We used twenty-eight male mice which equally and randomly were separated into four groups as follows: Control, DGL group (treated with 500 mg/kg/day DGL orally for six weeks), DGL + CTX group (treated with 500 mg/kg/day DGL orally plus 200 mg/kg/day CTX intraperitoneally for six weeks), and CTX group (treated with 200 mg/kg/day CTX intraperitoneally for six weeks). The liver and kidney function indices such as serum creatinine, blood urine nitrogen, alanine aminotransferase, and aspartate aminotransferase were measured. Also, levels of malondialdehyde, catalase, and glutathione peroxidase in hepatic and renal tissues were evaluated. Moreover, the expression profiles of interleukin 1 beta and tumor necrosis factor alpha were assessed. The liver and kidney tissues were assessed for histopathological lesions. The results showed that aging induced by DGL leads to abnormalities in functional indices of the liver and kidneys. DGL also induced significant oxidative stress and inflammation, as well as histopathological lesions, in these organs. CTX improved functional indices, as well as the parameters of oxidative stress and inflammation, compared with the DGL-treated animals. These results were also confirmed by histological evaluations of the liver and kidneys. These data provide evidence for the therapeutic value of CTX in clinical practice for mitigating the hepatorenal damages of aging.