scholarly journals Royal Jelly ameliorates 6-mercaptopurine induced spermatogenesis impairment and testicular apoptosis by regulating PI3K/AKT pathway in male rats

2020 ◽  
Author(s):  
khalid Hashem ◽  
Ahmed Z. Abdelazem ◽  
Naglaa W. Abdelbaky
Keyword(s):  
Adverse Effect ◽  
Mrna Expression ◽  
Sex Hormones ◽  
Caspase 3 ◽  
Royal Jelly ◽  
Male Rats ◽  
Akt Pathway ◽  
Albino Rats ◽  
Male Adult ◽  
Spermatogenesis Impairment

Abstract Testicular apoptosis is an obvious adverse effect of many chemotherapeutic agents.one of these chemotherapeutic drugs is 6-mercaptopurine (6MP) which has a powerful anticancer effect. On the contrary, it has an adverse effect on the male reproductive system. This study aimed to evaluate the prospective ameliorative effects of Royal Jelly (RJ) on 6MP induced testicular apoptosis and investigate the mechanistic pathway of protection. For this aim, forty male adult albino rats were divided into four equal groups (n= 10): control rats, RJ group (200 mg/kg.b.wt. of RJ for 30 day P.o.), 6MP group (5 mg/kg.b.wt of 6MP for 20 day P.o.), and RJ+6MP group pretreated with RJ (200 mg/kg.b.wt. for 10 day P.o.), and continued with 6MP (5 mg/kg.b.wt, P.o) for 20 day. After 30 days blood samples, epididymis and testis were collected to investigate sex hormones, sperm parameters, histological and molecular changes of testicular tissues, that include anti-oxidants activity, caspase-3, TNF-α, gene expression of Androgen receptors (AR) and P53 also protein concentration of PI3K, AKT, Nrf2 and HO1were estimated. The results of our study revealed that Pretreatment of Royal Jelly (RJ) abrogated 6MP induced spermatogenesis impairment by ameliorating sperm count, motility and morphology, regulating AR mRNA expression and sex hormones levels. RJ ameliorated testicular damage of 6MP exposed rats through restoring testicular antioxidant/oxidative redox, inhibiting caspase-3 activity and P53 mRNA expression as well as regulation of PI3K, AKT, Nrf2 and HO1 protein levels. Our data concluded that RJ protected testicular tissue from 6MP induced apoptosis by regulation PI3K/AKT pathway.

scholarly journals Royal Jelly ameliorates 6-mercaptopurine induced spermatogenesis impairment and testicular apoptosis by regulating PI3K/AKT pathway in male rats

2020 ◽  
Author(s):  
khalid Hashem ◽  
Ahmed Z. Abdelazem ◽  
Naglaa W. Abdelbaky
Keyword(s):  
Adverse Effect ◽  
Mrna Expression ◽  
Sex Hormones ◽  
Caspase 3 ◽  
Royal Jelly ◽  
Male Rats ◽  
Akt Pathway ◽  
Albino Rats ◽  
Male Adult ◽  
Spermatogenesis Impairment

Abstract Testicular apoptosis is an obvious adverse effect of many chemotherapeutic agents.one of these chemotherapeutic drugs is 6-mercaptopurine (6MP) which has a powerful anticancer effect. On the contrary, it has an adverse effect on the male reproductive system. This study aimed to evaluate the prospective ameliorative effects of Royal Jelly (RJ) on 6MP induced testicular apoptosis and investigate the mechanistic pathway of protection. For this aim, forty male adult albino rats were divided into four equal groups (n= 10): control rats, RJ group (200 mg/kg.b.wt. of RJ for 30 day P.o.), 6MP group (5 mg/kg.b.wt of 6MP for 20 day P.o.), and RJ+6MP group pretreated with RJ (200 mg/kg.b.wt. for 10 day P.o.), and continued with 6MP (5 mg/kg.b.wt, P.o) for 20 day. After 30 days blood samples, epididymis and testis were collected to investigate sex hormones, sperm parameters, histological and molecular changes of testicular tissues, that include anti-oxidants activity, caspase-3, TNF-α, gene expression of Androgen receptors (AR) and P53 also protein concentration of PI3K, AKT, Nrf2 and HO1were estimated. The results of our study revealed that Pretreatment of Royal Jelly (RJ) abrogated 6MP induced spermatogenesis impairment by ameliorating sperm count, motility and morphology, regulating AR mRNA expression and sex hormones levels. RJ ameliorated testicular damage of 6MP exposed rats through restoring testicular antioxidant/oxidative redox, inhibiting caspase-3 activity and P53 mRNA expression as well as regulation of PI3K, AKT, Nrf2 and HO1 protein levels. Our data concluded that RJ protected testicular tissue from 6MP induced apoptosis by regulation PI3K/AKT pathway.

scholarly journals Structural Characterization and Antioxidant Activity of Polysaccharides from Athyrium multidentatum (Doll.) Ching in d-Galactose-Induced Aging Mice via PI3K/AKT Pathway

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3364 ◽  
Author(s):  
Liang Jing ◽  
Jing-Ru Jiang ◽  
Dong-Mei Liu ◽  
Ji-Wen Sheng ◽  
Wei-Fen Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Molecular Weight ◽  
Protein Expression ◽  
Mrna Expression ◽  
Caspase 3 ◽  
Akt Pathway ◽  
Protective Mechanism ◽  
Related Factor ◽  
Bax Protein ◽  
Gene And Protein Expression

The purpose of this study was to characterize the polysaccharides from Athyrium multidentatum (Doll.) Ching (AMC) rhizome and explore the protective mechanism against d-galactose-induced oxidative stress in aging mice. Methods: A series of experiments, including molecular weight, monosaccharide composition, Fourier transform infrared (FT-IR) spectroscopy, and 1H nuclear magnetic resonance (1H NMR) spectroscopy were carried out to characterize AMC polysaccharides. The mechanism was investigated exploring d-galactose-induced aging mouse model. Quantitative real-time reverse transcription polymerase chain reaction (RT-qPCR) and western blotting assays were performed to assess the gene and protein expression in liver. Key findings: Our results showed that AMC polysaccharides were mainly composed of mannose (Man), rhamnose (Rha), glucuronic acid (Glc A), glucose (Glc), galactose (Gal), arabinose (Ara), and fucose (Fuc) in a molar ratio of 0.077:0.088:0.09:1:0.375:0.354:0.04 with a molecular weight of 33203 Da (Mw). AMC polysaccharides strikingly reversed d-galactose-induced changes in mice, including upregulated phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor-erythroid 2-related factor 2 (Nrf2), forkhead box O3a (FOXO3a), and hemeoxygenase-1 (HO-1) mRNA expression, raised Bcl-2/Bax ratio, downregulated caspase-3 mRNA expression, enhanced Akt, phosphorylation of Akt (p-Akt), Nrf2 and HO-1 protein expression, decreased caspase-3, and Bax protein expression. Conclusion: AMC polysaccharides attenuated d-galactose-induced oxidative stress and cell apoptosis by activating the PI3K/AKT pathway, which might in part contributed to their anti-aging activity.

scholarly journals Momordica charantia Extract Protects against Diabetes-Related Spermatogenic Dysfunction in Male Rats: Molecular and Biochemical Study

Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5255
Author(s):  
Gamal A. Soliman ◽  
Rehab F. Abdel-Rahman ◽  
Hanan A. Ogaly ◽  
Hassan N. Althurwi ◽  
Reham M. Abd-Elsalam ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Caspase 3 ◽  
Biochemical Study ◽  
Glycosylated Hemoglobin ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Momordica Charantia ◽  
Male Rats ◽  
Blood Levels ◽  
Diabetic Patients

More than 90% of diabetic patients suffer from sexual dysfunction, including diminished sperm count, sperm motility, and sperm viability, and low testosterone levels. The effects of Momordica charantia (MC) were studied by estimating the blood levels of insulin, glucose, glycosylated hemoglobin (HbA1c), testosterone (TST), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) in diabetic rats treated with 250 and 500 mg/kg b.w. of the total extract. Testicular antioxidants, epididymal sperm characteristics, testicular histopathology, and lesion scoring were also investigated. Testicular mRNA expression of apoptosis-related markers such as antiapoptotic B-cell lymphoma-2 (Bcl-2) and proapoptotic Bcl-2-associated X protein (Bax) were evaluated by real-time PCR. Furthermore, caspase-3 protein expression was evaluated by immunohistochemistry. MC administration resulted in a significant reduction in blood glucose and HbA1c and marked elevation of serum levels of insulin, TST, and gonadotropins in diabetic rats. It induced a significant recovery of testicular antioxidant enzymes, improved histopathological changes of the testes, and decreased spermatogenic and Sertoli cell apoptosis. MC effectively inhibited testicular apoptosis, as evidenced by upregulation of Bcl-2 and downregulation of Bax and caspase-3. Moreover, reduction in apoptotic potential in MC-treated groups was confirmed by reduction in the Bax/Bcl-2 mRNA expression ratio.

scholarly journals Male-specific suppression of hepatic microsomal UDP-glucuronosyl transferase activities toward sex hormones in the adult male rat administered bisphenol A

2002 ◽  
Vol 368 (3) ◽  
pp. 783-788 ◽  
Author(s):  
Noriaki SHIBATA ◽  
Junya MATSUMOTO ◽  
Ken NAKADA ◽  
Akira YUASA ◽  
Hiroshi YOKOTA
Keyword(s):  
Bisphenol A ◽  
Mrna Expression ◽  
Sex Hormones ◽  
Adult Male ◽  
Endocrine Disruptor ◽  
Liver Microsomes ◽  
Female Rats ◽  
Male Rats ◽  
Male Rat ◽  
Blotting Analysis

Various adverse effects of endocrine disruptors on the reproductive organs of male animals have been reported. We found that UDP-glucuronosyltransferase (UGT) activities towards bisphenol A, testosterone and oestradiol were significantly decreased in liver microsomes prepared from adult male Wistar rats administered with the endocrine disruptor bisphenol A (1mg/2 days for 2 or 4 weeks). However, suppression of the transferase activities was not observed in female rats, even after bisphenol A treatment for 4 weeks. Diethylstilbestrol, which is well known as an endocrine disruptor, had the same effects, but p-cumylphenol had no effect on UGT activities towards sex hormones. Co-administration of an anti-oestrogen, tamoxifen, inhibited the suppression of the transferase activities by bisphenol A. Western blotting analysis showed that the amount of UGT2B1, an isoform of UGT which glucuronidates bisphenol A, was decreased in the rat liver microsomes by the treatment. Northern blotting analysis also indicated that UGT2B1 mRNA in the liver was decreased by bisphenol A treatment. The suppression of UGT activities, UGT2B1 protein and UGT2B1 mRNA expression did not occur in female rats. The results indicate that bisphenol A treatment reduces the mRNA expression of UGT2B1 and other UGT isoforms that mediate the glucuronidation of sex hormones in adult male rats, and this suggests that the endocrine balance may be disrupted by suppression of glucuronidation.

scholarly journals Ameliorating Iron Overload in Intestinal Tissue of Adult Male Rats: Quercetin vs Deferoxamine

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Arwa A. El-Sheikh ◽  
Shimaa Hamed Ameen ◽  
Samaa Salah AbdEl-Fatah
Keyword(s):  
Oxidative Stress ◽  
Iron Overload ◽  
Adult Male ◽  
Caspase 3 ◽  
Iron Chelation ◽  
Male Rats ◽  
Albino Rats ◽  
Tissue Iron ◽  
Small Intestinal

Objective. The aim of our study is to compare the role of the new natural alternative (Quercetin) with the current iron-chelation therapy (Deferoxamine (DFO)) in the effect of iron overload on small intestinal tissues and to investigate the possible underlying molecular mechanisms of such toxicity. Methods. Forty-two adult male albino rats were divided into six groups: control groups, DFO, Quercetin, iron overload, iron overload+DFO, and iron overload+Quercetin groups. Animals received daily intraperitoneal injection of Deferoxamine (125 mg /kg), Quercetin (10 mg/kg), and ferric dextran (200 mg/kg) for 2 weeks. Results. Iron overloaded group showed significant increase in serum iron, total iron binding capacity (TIBC), transferrin saturation percentage (TS %) hepcidin (HEPC), serum ferritin, nontransferrin bound iron (NTBI), and small intestinal tissues iron levels. Iron overload significantly increased the serum oxidative stress indicator (MDA) and reduced serum total antioxidant capacity (TAC). On the other hand, iron overload increased IL6 and reduced IL10 in small intestinal tissues reflecting inflammatory condition and increased caspase 3 reactivity indicating apoptosis and increased iNOs expressing cell indicting oxidative stress especially in ileum. In addition, it induced small intestinal tissues pathological alterations. The treatment with Quercetin showed nonsignificant differences as compared to treatment with DFO that chelated the serum and tissue iron and improved the oxidative stress and reduced tissue IL6 and increased IL10 and decreased caspase 3 and iNOs expressing cells in small intestinal tissues. Moreover, it ameliorated the iron overload induced pathological alterations. Conclusion. Our study showed the potential role of Quercetin as iron chelator like DFO in case of iron overload induced small intestinal toxicity in adult rats because of its serum and tissue iron chelation, improvement of serum, and small intestinal oxidative stress, ameliorating iron induced intestinal inflammation, apoptosis, and histopathological alterations.

Cadmium acts as a silent killer of liver by inducing oxidative stress and hepatocellular injury and a possible amelioration by vitamin B12 and folic acid in rat model

2019 ◽  
Vol 1 ◽  
pp. 105-117
Author(s):  
A. Banerjee ◽  
P. Nandi ◽  
C. Bhattacharya ◽  
Z. Kabir ◽  
S. Mukherjee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Folic Acid ◽  
Vitamin B12 ◽  
Rat Model ◽  
Male Rats ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Hepatocellular Injury ◽  
Male Adult ◽  
Wistar Albino Rats

<br/><b>Purpose:</b> To investigate the involvement of oxidative stress in Cadmium (Cd) induced alteration in the functional status of the liver. And to assess the efficacy of folic acid and vitamin B12 in preventing Cd-induced damage in the same. <br/><b>Materials and methods:</b> The experiment was carried out for four weeks. For the experiment, 25 healthy male adult Wistar albino rats were randomly selected and were divided into five equal groups and treated as control, treated with Cd, supplemented with vitamin B12 and folic acid and in the combination of these two. After 28 days the liver function enzymes and oxidative stress parameters were measured. <br/><b>Results:</b> Cd is the silent killer of the hepatic system through the induction of oxidative stress in male rats. From this investigation, it is evident that the folic acid+vitamin B12 possess significant hepatoprotective and antioxidant activity against Cd-induced hepatotoxicity in the rat model. In addition, results revealed that the folic acid alone and or in combination with vitamin B12 blunted the hepatotoxic effect significantly. <br/><b>Conclusions:</b> Based on results obtained, it can be concluded that folic acid and vitamin B12 offer a protective effect in Cd-induced oxidative stress associated with hepatocellular injury. Folic acid and vitamin B12 can be considered as a potent natural antioxidant which has the capacity to provide protection against Cd-induced oxidative stress in the liver in rats. However, to elucidate the exact mechanism of this modulatory effect and to examine its potential therapeutic effects further studies are essential.

scholarly journals Protective Role of Rockect Seed (Eruca sativa) Extract against Monosodium Glutamate-induced Hepato-renal Toxicity in Male Rats

2020 ◽  
pp. 1-10
Author(s):  
Ehab Tousson ◽  
Afaf El-Atrash ◽  
Yosra Karson
Keyword(s):  
Renal Damage ◽  
Renal Toxicity ◽  
Monosodium Glutamate ◽  
Chloride Ions ◽  
Male Rats ◽  
Male Rat ◽  
Albino Rats ◽  
Male Adult ◽  
Liver And Kidney

Background and Objective: Monosodium glutamate (MSG) is identified as an Accent that is used in the food industry as a flavour enhancer with an umami taste that intensifies the meaty, savoury flavour of food. The present study aimed at evaluating the protective and ameliorative role of rocket seeds extract against monosodium glutamate-induced hepatic renal toxicity and oxidative stress in the male rat. Materials and Methods: A total of 60 male adult albino rats were equally divided into six groups (G1, Control; G2, rocket seeds (RS); G3, ACCENT or MSG; G4, Co- treated (RS+MSG); G5, Post- treated (MSG+RS); G6, Self-treated MSG).  Results: Current results revealed that; a significant increase in serum ALT, AST, ALP, AFP, Urea, Creatinine, potassium ions, chloride ions, cholesterol, triglyceride, HDL, and LDL levels in MSG as compared to control and RS groups. In contrast; a significant decrease in serum albumin, total proteins, catalase, GSH and SOD in liver and kidney homogenates in MSG as compared to control and RS groups. Co- or post-treatment of MSG with rocket seeds improved this change in liver and kidney functions, with best results for co-treatment than post and self-treatment. Conclusion: These findings suggested that the misuse of monosodium glutamate may contribute to continuous hepatic and renal damage. This shows that the desired dose of monosodium glutamate can safely be used with grapes seed in improving hepatic and renal damage in monosodium glutamate in young rats.

scholarly journals Role of Oats in Ameliorating Hepatic and Renal Toxicity Induced by Acute Lead Nanoparticles in Male Rats

2020 ◽  
pp. 38-45
Author(s):  
Sarah Alashmouni ◽  
Afaf El- Atrash ◽  
Manar Kandeel ◽  
Ehab Tousson
Keyword(s):  
Renal Damage ◽  
Chloride Ions ◽  
The Body ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Sufficient Information ◽  
Therapeutic Effects ◽  
Male Adult ◽  
Organ Systems

Aims: Lead is well known environmental pollutant, which can cause toxic effects in multiple organ systems. Lead originates from various industrial and/or household sources, and enters the body through food and fluid intakes, as well as by inhalation. No sufficient information present about the toxic effect of acute lead nanoparticles on kidney and liver. Accordingly, current study was performed to study the therapeutic effects of Oats extract towards the injection of lead nanoparticles (Pb NPs) in rat induced kidney and liver damage by increasing kidney and liver functions, and electrolytes. Study Design:  A total of 40 male adult albino rats were equally divided into four groups (Control group, Oats group, Pb NPs group as acute toxicity and last group is Pb NPs +Oats). Results: Current results revealed that; a significant increase in the levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), alkaline phosphatase (ALP), urea, creatinine, potassium and chloride ions after injection with Pb NPs as compared to control group. In contrast; a significant decrease in serum albumin, total proteins, and sodium ions in Pb NPs as compared to control groups. Treatment of Pb NPs with Oats improved this change in liver and kidney functions as compared to Pb NPs group. Conclusion: These findings suggested that; lead nanoparticles injection induced hepatic and renal damage. This shows that the desired dose of Pb NPs can safely be used with Oats in improving hepatic and renal damage in toxic group in young rats.

scholarly journals Ginkgo biloba Alleviates Cisplatin-Mediated Neurotoxicity in Rats via Modulating APP/Aβ/P2X7R/P2Y12R and XIAP/BDNF-Dependent Caspase-3 Apoptotic Pathway

2020 ◽  
Vol 10 (14) ◽  
pp. 4786
Author(s):  
Dina H. Gomaa ◽  
Walaa G. Hozayen ◽  
Haidy Al-shafeey ◽  
Asmaa Mohammed M. Hussein Elkelawy ◽  
Khalid S. Hashem
Keyword(s):  
Adverse Effect ◽  
Body Weight ◽  
Ginkgo Biloba ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Amyloid Β ◽  
Control Group ◽  
Albino Rats ◽  
Apoptotic Pathway ◽  
Apoptotic Effect

Neurotoxicity is an obvious adverse effect in Patients encountering a complete course of chemotherapy. The present work is conducted to evaluate the neuroprotective effect of Ginkgo biloba (Ginkgo) against the neurotoxicity induced by Cisplatin (Cis) in rats. Forty male Wistar albino rats were arranged into four groups: (1) Control group, rats were given saline; (2) Cis group, rats were injected by Cis 2 mg/kg body weight i.p., twice a week starting on the fifth day for thirty days; (3) Ginkgo group, rats were administered Ginkgo (50 mg/kg orally) daily for thirty days; and (4) Ginkgo+Cis group, rats received Ginkgo (50 mg/kg orally) daily and on the fifth day, rats were injected with Cis (2 mg/Kg body weight i.p.) twice a week for thirty days. Cis significantly increased Gamma glutamyltransferase (GGT) and Acetyl Cholinesterase (CHE) as compared to the control group and also disturbed cerebral oxidative/antioxidant redox. Co-administration of Ginkgo and Cis reversed the adverse effect of Cis on the brain tissue. Moreover, co-administration of Ginkgo and Cis ameliorated Cis induced brain damage by reducing Amyloid precursor protein (APP), amyloid β (Aβ), P2Y12R and P2X7R mRNA expressions and proteins. Furthermore, Ginkgo regulated XIAP/BDNF expressions with a consequent decrease of caspase-3 and DNA fragmentation%. The current results concluded that concurrent treatment with Ginkgo can mitigate neurotoxicity mediated by Cis in experimental animals through exhibiting antioxidant effect by restoring cerebral oxidative/antioxidant redox and anti-apoptotic effect via regulating cerebral APP/Aβ/P2Y12R/P2X7R and XIAP/BDNF signaling pathways.

scholarly journals Ameliorative Role of Cerium Oxide Nanoparticles Against Fipronil Impact on Brain Function, Oxidative Stress, and Apoptotic Cascades in Albino Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Norhan Elshony ◽  
Atef M. K. Nassar ◽  
Yasser S. El-Sayed ◽  
Dalia Samak ◽  
Ahmed Noreldin ◽  
...  
Keyword(s):  
Cerium Oxide ◽  
Brain Function ◽  
Caspase 3 ◽  
B Cell Lymphoma ◽  
Male Rats ◽  
Cerium Oxide Nanoparticles ◽  
Albino Rats ◽  
Oxide Nanoparticles ◽  
Wide Range ◽  
Brain Tissues

Fipronil (FIP) is an N-phenylpyrazole insecticide that is used extensively in public health and agriculture against a wide range of pests. Exposure to FIP is linked to negative health outcomes in humans and animals including promoting neuronal cell injury, which results in apoptosis through the production of reactive oxygen species (ROS). Therefore, the purpose of the current study was to investigate the neuroprotective effects of cerium oxide nanoparticles (CeNPs) on neuronal dysfunction induced by FIP in albino rats. Male rats were randomly classified into four groups: control, FIP (5 mg/kg bwt), CeNPs (35 mg/kg bwt), and FIP + CeNPs (5 (FIP) + 35 (CeNPs) mg/kg bwt), which were treated orally once daily for 28 consecutive days. Brain antioxidant parameters, histopathology, and mRNA expression of genes related to brain function were evaluated. The results revealed oxidative damage to brain tissues in FIP-treated rats indicated by the elevated levels of malondialdehyde (MDA) and nitric oxide (NO) levels and reduced activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx). On the other hand, the FIP’s group that was treated with CeNPs showed decrease in MDA and NO levels and increase in SOD and GPx enzymes activity. Besides, FIP-treated rats showed decreased butyrylcholinesterase (BuChE) activity in comparison to the FIP + CeNPs group. Moreover, FIP caused up-regulation of the expression of neuron-specific enolase (NSE), caspase-3, and glial fibrillary acidic protein (GFAP) but down-regulation of B-cell lymphoma-2 (BCL-2) expression. But the FIP + CeNPs group significantly down-regulated the GFAP, NSE, and caspase-3 and up-regulated the gene expression of BCL-2. Additionally, the FIP-treated group of rats had clear degenerative lesions in brain tissue that was reversed to nearly normal cerebral architecture by the FIP + CeNPs treatment. Immunohistochemical examination of brain tissues of rats-treated with FIP showed abundant ionized calcium-binding adaptor molecule 1 (Iba-1) microglia and caspase-3 and apoptotic cells with nearly negative calbindin and synaptophysin reaction, which were countered by FIP + CeNPs treatment that revealed a critical decrease in caspase-3, Iba-1 reaction with a strong calbindin positive reaction in most of the Purkinje cells and strong synaptophysin reaction in the cerebrum and cerebellum tissues. Based on reported results herein, CeNPs treatment might counteract the neurotoxic effect of FIP pesticide via an antioxidant-mediated mechanism.

Sign in / Sign up

Export Citation Format

Share Document