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Article ; Online: Pioglitazone ameliorates DOX-induced cognitive impairment by mitigating inflammation, oxidative stress, and apoptosis of hippocampal neurons in rats.

Alhowail, Ahmad H

2023 Volume 457, Page(s) 114714

Abstract: Doxorubicin (DOX) is broadly used as a medication for cancer treatment. However, DOX has been connected with chemotherapy-related complications, for instance, cognitive impairment (chemobrain). Chemobrain developed in up to 70% of cancer patients; ... ...

Abstract	Doxorubicin (DOX) is broadly used as a medication for cancer treatment. However, DOX has been connected with chemotherapy-related complications, for instance, cognitive impairment (chemobrain). Chemobrain developed in up to 70% of cancer patients; therapeutic is unavailable. This study investigated the preventive effect of pioglitazone (PIO) on neurotoxicity caused by (DOX) in the hippocampus. Forty rats were separated into four groups; control (normal saline 10 ml/kg), DOX (5 mg/kg, intraperitoneally every 3rd day, equivalent to 20 mg/kg cumulative dose), PIO (2 mg/kg in drinking water), and DOX+PIO (DOX, 5 mg/kg, intraperitoneally every 3rd day concurrently PIO, 2 mg/kg in drinking water) and duration of drug treatment lasted for 14 days. The animals were subjected to contextual fear memory tests to characterize the cognitive impairment following DOX treatment. ELISA assessed hippocampal protein expression related to inflammation, oxidative damage, and apoptosis. DOX-treatment produced significant reduction in freezing duration in contextual fear memory tests, which was reversed by PIO co-administration. DOX increased neuroinflammation, oxidative stress, apoptosis, and mitochondrial activity by increasing NF-κB and COX-2 levels, reducing SOD levels, and increasing Bax, caspase-3, and lipid peroxidation. However, DOX did not affect GSH or catalase levels. PIO co-administration reduces NF-κB, COX-2, MDA, Bax, and caspase-3 levels and improves mitochondrial activity and SOD expression. To sum up, DOX therapy accelerates cognitive decline in rats by increasing neuroinflammation, oxidative stress, mitochondrial dysfunction, lipid peroxidation, and apoptosis. PIO is a promising treatment for DOX-induced cognitive impairment.
MeSH term(s)	Humans ; Rats ; Animals ; Pioglitazone/pharmacology ; Caspase 3/metabolism ; bcl-2-Associated X Protein/metabolism ; Chemotherapy-Related Cognitive Impairment ; NF-kappa B/metabolism ; Neuroinflammatory Diseases ; Cyclooxygenase 2/metabolism ; Drinking Water/adverse effects ; Drinking Water/metabolism ; Doxorubicin/toxicity ; Oxidative Stress ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/metabolism ; Apoptosis ; Inflammation/chemically induced ; Inflammation/drug therapy ; Inflammation/metabolism ; Hippocampus/metabolism ; Neurons/metabolism ; Superoxide Dismutase/metabolism
Chemical Substances	Pioglitazone (X4OV71U42S) ; Caspase 3 (EC 3.4.22.-) ; bcl-2-Associated X Protein ; NF-kappa B ; Cyclooxygenase 2 (EC 1.14.99.1) ; Drinking Water ; Doxorubicin (80168379AG) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2023-10-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2023.114714
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Article: Doxorubicin impairs cognitive function by upregulating AMPAR and NMDAR subunit expression and increasing neuroinflammation, oxidative stress, and apoptosis in the brain.

Alhowail, Ahmad H / Aldubayan, Maha A

Frontiers in pharmacology

2023 Volume 14, Page(s) 1251917

Abstract: Introduction: ...

Abstract	Introduction:
Language	English
Publishing date	2023-11-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2023.1251917
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Article: The Impact of Metformin on the Development of Hypothyroidism and Cardiotoxicity Induced by Cyclophosphamide, Methotrexate, and Fluorouracil in Rats.

Alhowail, Ahmad H / Aldubayan, Maha A

Pharmaceuticals (Basel, Switzerland)

2023 Volume 16, Issue 9

Abstract: Cyclophosphamide (CYP), methotrexate (MTX), and 5-fluorouracil (5-FU) are extensively utilized in the therapeutic management of various malignancies. It is noteworthy, however, that potential chemotherapy-related complications include the occurrence of ... ...

Abstract	Cyclophosphamide (CYP), methotrexate (MTX), and 5-fluorouracil (5-FU) are extensively utilized in the therapeutic management of various malignancies. It is noteworthy, however, that potential chemotherapy-related complications include the occurrence of hypothyroidism and cardiotoxicity. Metformin (MET) is a pharmacological agent for managing type 2 diabetes. It has been reported to mitigate certain toxic manifestations associated with chemotherapy. This study's primary objective is to investigate MET's protective effects against hypothyroidism and cardiotoxicity induced by CMF treatment. A total of forty male rats were allocated into four distinct groups, each consisting of ten rats per group. These groups were categorized as follows: saline, MET, CMF, and CMF + MET. The experimental group of rats were administered CMF via intraperitoneal injection, receiving two doses of CMF, and fed MET in their daily drinking water, with a 2.5 mg/mL concentration. Blood samples were collected into EDTA tubes for assessment of TSH, free and total (T4 and T3), troponin I, CK, and CK-MB levels utilizing Electrochemiluminescence Immunoassays (ECI). The saline and MET groups did not exhibit significant alterations in thyroid hormones or cardiotoxic biomarkers. In contrast, in the CMF group, there was a notable reduction in T4, FT4, T3, and FT3 levels but no significant changes in TSH levels; however, troponin I, CK, and CK-MB levels were notably elevated. MET co-treatment with CMF did not ameliorate these effects caused by CMF. In conclusion, CMF treatment induced hypothyroidism and cardiotoxicity in rats, but MET co-treatment did not rescue the reduction of thyroid hormones or the elevation of cardiotoxic biomarkers.
Language	English
Publishing date	2023-09-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph16091312
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Article ; Online: The Ameliorative Effect of Pioglitazone against Neuroinflammation Caused by Doxorubicin in Rats.

Alsaud, May M / Alhowail, Ahmad H / Aldubayan, Maha A / Almami, Ibtesam S

Molecules (Basel, Switzerland)

2023 Volume 28, Issue 12

Abstract: Doxorubicin (DOX) is a chemotherapeutic agent that is linked with complications such as cardiotoxicity and cognitive dysfunction, known as chemobrain. Chemobrain affects up to 75% of cancer survivors, and there are no known therapeutic options for its ... ...

Abstract	Doxorubicin (DOX) is a chemotherapeutic agent that is linked with complications such as cardiotoxicity and cognitive dysfunction, known as chemobrain. Chemobrain affects up to 75% of cancer survivors, and there are no known therapeutic options for its treatment. This study aimed to determine the protective effect of pioglitazone (PIO) against DOX-induced cognitive impairment. Forty Wistar female rats were equally divided into four groups: control, DOX-treated, PIO-treated, and DOX + PIO-treated. DOX was administered at a dose of 5 mg/kg, i.p., twice a week for two weeks (cumulative dose, 20 mg/kg). PIO was dissolved in drinking water at a concentration of 2 mg/kg in the PIO and DOX-PIO groups. The survival rates, change in body weight, and behavioral assessment were performed using Y-maze, novel object recognition (NOR), and elevated plus maze (EPM), followed by estimation of neuroinflammatory cytokines IL-6, IL-1β, and TNF-α in brain homogenate and RT-PCR of a brain sample. Our results showed a survival rate of 40% and 65% in the DOX and DOX + PIO groups, respectively, compared with a 100% survival rate in the control and PIO treatment groups at the end of day 14. There was an insignificant increase in body weight in the PIO group and a significant reduction in the DOX and DOX + PIO groups as compared with the control groups. DOX-treated animals exhibited impairment of cognitive function, and the combination PIO showed reversal of DOX-induced cognitive impairment. This was evidenced by changes in IL-1β, TNF-α, and IL-6 levels and also by mRNA expression of TNF- α, and IL-6. In conclusion, PIO treatment produced a reversal of DOX-induced memory impairment by alleviating neuronal inflammation by modulating the expression of inflammatory cytokines.
MeSH term(s)	Rats ; Female ; Animals ; Pioglitazone/pharmacology ; Rats, Wistar ; Neuroinflammatory Diseases ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/pharmacology ; Interleukin-6/genetics ; Interleukin-6/pharmacology ; Chemotherapy-Related Cognitive Impairment ; Doxorubicin/pharmacology ; Cytokines/pharmacology ; Body Weight ; Oxidative Stress
Chemical Substances	Pioglitazone (X4OV71U42S) ; Tumor Necrosis Factor-alpha ; Interleukin-6 ; Doxorubicin (80168379AG) ; Cytokines
Language	English
Publishing date	2023-06-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1413402-0
ISSN	1420-3049 ; 1431-5165 ; 1420-3049
ISSN (online)	1420-3049
ISSN	1431-5165 ; 1420-3049
DOI	10.3390/molecules28124775
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Article: Protective Effect of Galantamine against Doxorubicin-Induced Neurotoxicity.

Alsikhan, Rawan S / Aldubayan, Maha A / Almami, Ibtesam S / Alhowail, Ahmad H

Brain sciences

2023 Volume 13, Issue 6

Abstract: Background and aims: Doxorubicin (DOX) causes cognitive impairment (chemobrain) in patients with cancer. While DOX damages the cholinergic system, few studies have focused on the protective effects of cholinergic function on chemobrain. The ... ...

Abstract	Background and aims: Doxorubicin (DOX) causes cognitive impairment (chemobrain) in patients with cancer. While DOX damages the cholinergic system, few studies have focused on the protective effects of cholinergic function on chemobrain. The acetylcholinesterase inhibitor galantamine (GAL) demonstrates neuroprotective properties. We investigated the mechanisms associated with DOX-induced cognitive impairments and the potential protective role of GAL in preventing chemobrain. Main methods: Female Wistar rats were divided into control, DOX, GAL, and DOX + GAL groups. The rats in the DOX group were administered DOX (5 mg/kg intraperitoneally twice weekly for two weeks), while those in the GAL group were orally administered GAL (2.5 mg/kg) via oral gavage once daily for 15 days. The combination group (DOX + GAL) received GAL (once daily) and DOX (two times per week) concurrently. The body weights and survival rates were monitored daily. The animals were subjected to behavioral tests to assess the memory function followed by the biochemical estimation of inflammatory markers, including tumor necrosis factor-α (TNF- Key findings: DOX caused a reduction in the body weight and survival rate, which was alleviated by GAL concomitant treatment with DOX (DOX + GAL). These groups had reduced body weights and survival rates. DOX-treated animals exhibited an impairment of short-term spatial working memory, manifested as a behavioral alteration in the Y-maze test, the novel object recognition (NOR) test, and the elevated plus-maze (EPM) test. Concurrent treatment with GAL (DOX + GAL) showed improved memory function, as evidenced by an increase in the number of entries and time spent in the novel arm, the time spent exploring the novel object, and the transfer latency in the Y-maze, NOR test, and EPM test, respectively. These findings were also supported by biochemical observations showing the reversal of DOX-induced changes in IL-1 Conclusion: GAL appeared to be a neuroprotective agent against neuroinflammation caused by DOX by reducing inflammatory markers in the brain.
Language	English
Publishing date	2023-06-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci13060971
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Article ; Online: Development of Diphenyl carbonate-Crosslinked Cyclodextrin Based Nanosponges for Oral Delivery of Baricitinib: Formulation, Characterization and Pharmacokinetic Studies.

Aldawsari, Mohammed F / Alhowail, Ahmad H / Anwer, Md Khalid / Ahmed, Mohammed Muqtader

International journal of nanomedicine

2023 Volume 18, Page(s) 2239–2251

Abstract: Background: The aim of the present investigation is to prepare baricitinib (BAR)-loaded diphenyl carbonate (DPC) β-cyclodextrin (βCD) based nanosponges (NSs) to improve the oral bioavailability.: Methods: BAR-loaded DPC-crosslinked βCD NSs (B-DCNs) ... ...

Abstract	Background: The aim of the present investigation is to prepare baricitinib (BAR)-loaded diphenyl carbonate (DPC) β-cyclodextrin (βCD) based nanosponges (NSs) to improve the oral bioavailability. Methods: BAR-loaded DPC-crosslinked βCD NSs (B-DCNs) were prepared prepared by varying the molar ratio of βCD: DPC (1:1.5 to 1:6). The developed B-DCNs loaded with BAR were characterized for particle size, polydispersity index (PDI), zeta potential (ZP), % yield and percent entrapment efficiency (%EE). Results: Based on the above evaluations, BAR-loaded DPC βCD NSs (B-CDN3) was optimized with mean size (345.8±4.7 nm), PDI (0.335±0.005), Yield (91.46±7.4%) and EE (79.1±1.6%). The optimized NSs (B-CDN3) was further confirmed by SEM, spectral analysis, BET analysis, in vitro release and pharmacokinetic studies. The optimized NSs (B-CDN3) showed 2.13 times enhancement in bioavailability in comparison to pure BAR suspension. Conclusion: It could be anticipated that NSs loaded with BAR as a promising tool for release and bioavailability for the treatment of rheumatic arthritis and Covid-19.
MeSH term(s)	Humans ; Cyclodextrins ; COVID-19 ; COVID-19 Drug Treatment
Chemical Substances	baricitinib (ISP4442I3Y) ; diphenyl (2L9GJK6MGN) ; Cyclodextrins
Language	English
Publishing date	2023-04-27
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2364941-0
ISSN	1178-2013 ; 1176-9114
ISSN (online)	1178-2013
ISSN	1176-9114
DOI	10.2147/IJN.S405534
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Article ; Online: Comparative evaluation of doxorubicin, cyclophosphamide, 5-fluorouracil, and cisplatin on cognitive dysfunction in rats: Delineating the role of inflammation of hippocampal neurons and hypothyroidism.

Alotayk, Lamis I / Aldubayan, Maha A / Alenezi, Sattam K / Anwar, Md Jamir / Alhowail, Ahmad H

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 165, Page(s) 115245

Abstract: Chemotherapeutic agents such as doxorubicin, cyclophosphamide, fluorouracil, and cisplatin are commonly used to treat a variety of cancers and often result in chemobrain, which manifests as difficulties in learning and memory processes that can persist ... ...

Abstract	Chemotherapeutic agents such as doxorubicin, cyclophosphamide, fluorouracil, and cisplatin are commonly used to treat a variety of cancers and often result in chemobrain, which manifests as difficulties in learning and memory processes that can persist in the years following treatment. The current study aims to evaluate the cognitive function following treatment with these agents and the underlying mechanisms using a rat model of neuroinflammation and possible implication of thyroid toxicity in chemotherapy induced cognitive dysfunction. Wistar female rats were treated with a single dose of doxorubicin (DOX, 25 mg/kg), 5-fluorouracil (5-FU, 100 mg/kg), cisplatin (8 mg/kg), and cyclophosphamide (CYP, 200 mg/kg) by intraperitoneal injection. The cognitive performance of rats was then evaluated in spatial memory tasks using the Y-maze, novel object recognition (NOR), and elevated plus maze (EPM) tests. Serum levels of thyroid hormones (T3, T4, FT3, and FT4) and thyroid stimulating hormone (TSH) were measured, followed by estimation of TNFα, IL-6, and IL-1β in the hippocampal tissue. Results revealed that all the chemotherapeutic agents produced impairment of cognitive function, and significant increase of pro-inflammatory cytokines such as TNFα, IL-6 and IL-1β in the hippocampal tissues. There was a significant reduction in thyroid hormones (T3, FT3, and T4) and an increase in thyroid stimulating hormone (TSH) in serum, which may also have contributed to the decline in cognitive function. In conclusion, DOX, 5-FU, CYP, and cisplatin produces impairment of spatial memory possibly by inflammation of hippocampal neurons and endocrine disruption (hypothyroidism) in rats.
MeSH term(s)	Rats ; Female ; Animals ; Fluorouracil/adverse effects ; Cisplatin/toxicity ; Tumor Necrosis Factor-alpha/adverse effects ; Interleukin-6 ; Rats, Wistar ; Cyclophosphamide/toxicity ; Cognitive Dysfunction/chemically induced ; Doxorubicin/toxicity ; Hypothyroidism/chemically induced ; Hippocampus ; Thyroid Hormones ; Thyrotropin ; Inflammation/chemically induced ; Neurons
Chemical Substances	Fluorouracil (U3P01618RT) ; Cisplatin (Q20Q21Q62J) ; Tumor Necrosis Factor-alpha ; Interleukin-6 ; Cyclophosphamide (8N3DW7272P) ; Doxorubicin (80168379AG) ; Thyroid Hormones ; Thyrotropin (9002-71-5)
Language	English
Publishing date	2023-07-29
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.115245
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Article ; Online: Health status outcome among cannabis addicts after treatment of addiction.

Siwar, Mohammed Ali A L / Mansour, Sayed Hossam El-Din / Aldubayan, Maha A / Alhowail, Ahmad H / Almogbel, Yasser S / Emara, Ashraf Mahmoud

PloS one

2023 Volume 18, Issue 11, Page(s) e0290730

Abstract: The abuse of Cannabis is a widespread issue in the Asir region. It has a lot of legal and occupational repercussions. The purpose of this study was to evaluate the health status of cannabis addicts at admission and after treatment using body mass index, ... ...

Abstract	The abuse of Cannabis is a widespread issue in the Asir region. It has a lot of legal and occupational repercussions. The purpose of this study was to evaluate the health status of cannabis addicts at admission and after treatment using body mass index, glycemic status, liver function, renal function, and oxidative stress. A cross-sectional study was conducted with 120 participants. The study was conducted at Al Amal Hospital for Mental Health in Asir region of Saudi Arabia, with 100 hospitalized patients receiving addiction treatment and 20 healthy volunteers. The participants were divided into two groups: group I, the control group, and group II, the cannabis addicts. The socio-demographic data were gathered. The level of cannabis in the urine and the CWAS [Cannabis Withdrawal Assessment Scale] were determined. In addition, the Body Mass Index [BMI], vital signs [temperature, heart rate, systolic blood pressure, diastolic blood pressure, and respiratory rate], serum levels of albumin, total bilirubin, direct bilirubin, AST, ALT, and ALP, urea, creatinine, Thiobarbituric acid-reactive substances [TBARS], superoxide dismutase [SOD], reduced glutathione [GSH], and catalase [CAT] were analyzed on the first day of admission and after treatment. According to the results, there was no significant change in the body mass index. The vital signs in the cannabis user group were significantly lower than the corresponding admission values. Regarding renal function tests such as urea and creatinine, we found that after treatment, the mean urea and creatinine values in the cannabis user group did not differ significantly from the corresponding admission values. However, after treatment, the mean values of fasting blood glucose levels in the cannabis user group were significantly lower than at admission. Also, the mean values of liver function tests such as albumin, total bilirubin, direct bilirubin, AST, ALT, and ALP in the cannabis user group were significantly lower than the corresponding admission values after treatment. In assessing the antioxidant system, we found that the mean values of TBARS, SOD, GSH, and CAT in the cannabis user group did not differ significantly from the corresponding admission values after treatment. The current findings have revealed that cannabis addiction harms the various body systems and has significant implications for the addict's state of health. The values of oxidative stress biomarkers did not change in this study, but other measured parameters improved after treatment.
MeSH term(s)	Humans ; Cannabis/adverse effects ; Cannabis/metabolism ; Thiobarbituric Acid Reactive Substances ; Creatinine ; Cross-Sectional Studies ; Antioxidants ; Catalase ; Oxidative Stress ; Bilirubin ; Glutathione ; Albumins ; Urea ; Health Status ; Superoxide Dismutase/metabolism ; Liver/metabolism
Chemical Substances	Thiobarbituric Acid Reactive Substances ; Creatinine (AYI8EX34EU) ; Antioxidants ; Catalase (EC 1.11.1.6) ; Bilirubin (RFM9X3LJ49) ; Glutathione (GAN16C9B8O) ; Albumins ; Urea (8W8T17847W) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0290730
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Article: Evaluation of Cisplatin-Induced Acute Renal Failure Amelioration Using Fondaparinux and Alteplase.

Abdel-Bakky, Mohamed S / Aldakhili, Anas S A / Ali, Hussein M / Babiker, Ali Y / Alhowail, Ahmad H / Mohammed, Salman A A

Pharmaceuticals (Basel, Switzerland)

2023 Volume 16, Issue 7

Abstract: Acute renal failure (ARF) is a deleterious condition with increased mortality or healthcare costs or dialysis-dependent end-stage renal disease. The study aims to compare prophylaxis with fondaparinux (Fund) vs. treatment with alteplase (Alt) in ... ...

Abstract	Acute renal failure (ARF) is a deleterious condition with increased mortality or healthcare costs or dialysis-dependent end-stage renal disease. The study aims to compare prophylaxis with fondaparinux (Fund) vs. treatment with alteplase (Alt) in ameliorating cisplatin (Cis)-induced ARF. Sixty male mice were equally divided randomly into six groups of control, Cis, Alt, and Cis + Alt groups receiving normal saline for 10 days. All four groups except for the control received Cis (30 mg/kg, i.p.) on day 7, and 6 h later, both the Alt groups received Alt (0.9 mg/kg, i.v.). The animal groups Fund and Fund + Cis received Fund (5 mg/kg, i.p.) for 10 days, and the Fund + Cis group on day 7 received Cis. All the animal groups were euthanized 72 h after the Cis dose. The Fund + Cis group showed significantly increased expression levels of platelet count, retinoid X receptor alpha (RXR-α) and phosphorylated Akt (p-Akt) in addition to decreased levels of urea, blood urea nitrogen (BUN), uric acid, white blood cells (WBCs), red blood cells (RBCs), relative kidney body weight, kidney injury score, glucose, prothrombin (PT), A Disintegrin And Metalloproteinases-10 (ADAM10), extracellular matrix deposition, protease-activated receptor 2 (PAR-2), and fibrinogen expression when compared to the Cis-only group. Meanwhile, the Cis + Alt group showed increased caspase-3 expression in addition to decreased levels of urea, BUN, uric acid, WBCs, RBCs, glucose, platelet count and PT expression with a marked decrease in PAR-2 protein expression compared to the Cis group. The creatinine levels for both the Fund + Cis and Cis + Alt groups were found to be comparable to those of the Cis-only group. The results demonstrate that the coagulation system's activation through the stimulation of PAR-2 and fibrinogen due to Cis-induced ADAM10 protein expression mediated the apoptotic pathway, as indicated by caspase-3 expression through the p-Akt pathway. This is normally accompanied by the loss of RXR-α distal and proximal tubules as lipid droplets. When the animals were pre-treated with the anticoagulant, Fund, the previous deleterious effect was halted while the fibrinolytic agent, Alt, most of the time failed to treat Cis-induced toxicity.
Language	English
Publishing date	2023-06-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph16070910
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Article ; Online: Vitamin B17 Ameliorates Methotrexate-Induced Reproductive Toxicity, Oxidative Stress, and Testicular Injury in Male Rats.

Felemban, Shatha G / Aldubayan, Maha A / Alhowail, Ahmad H / Almami, Ibtesam S

Oxidative medicine and cellular longevity

2020 Volume 2020, Page(s) 4372719

Abstract: Methotrexate (MTX; 4-amino-10-methylfolic acid) is a folic acid reductase inhibitor used to treat autoimmune diseases and certain types of cancer. Testicular toxicity resulting from MTX is a significant side effect that may cause subsequent infertility. ... ...

Abstract	Methotrexate (MTX; 4-amino-10-methylfolic acid) is a folic acid reductase inhibitor used to treat autoimmune diseases and certain types of cancer. Testicular toxicity resulting from MTX is a significant side effect that may cause subsequent infertility. The present study was conducted to examine the ameliorating effects of vitamin B17 (VitB17) against testicular toxicity induced by MTX in male rats. A total of 50 male albino rats were equally divided into five groups [control group; vitamin B17 group (VitB17) administered VitB17 only; methotrexate group administered MTX only; cotreated group, (VitB17+MTX) and posttreated group (MTX+VitB17)]. In methotrexate group (MTX), a significant decrease was observed in body weight and the testicular weight, as well as the levels of plasma testosterone, luteinizing hormone and follicle-stimulating hormone compared with control. The sperm count, viability, morphology index, total motility, and progressive motility also decreased in MTX rats compared with control. Furthermore, the levels of reduced glutathione, catalase, and superoxide dismutase, as well as proliferating cell nuclear antigen protein expression, in the testicular tissue decreased in MTX compared with control. In addition, MTX caused a significant increase in DNA and tissue damage compared with control. However, VitB17 ameliorated these effects, indicating that it has a preventative and curative effect against MTX-induced reproductive toxicity in male rats. The protective effect of VitB17 may be associated to its antioxidant properties as it possibly acts as a free-radical scavenger and lipid peroxidation inhibitor, as well as its protective effect on the levels of GSH, SOD, and CAT.
MeSH term(s)	Animals ; DNA Damage ; Male ; Methotrexate/adverse effects ; Methotrexate/pharmacology ; Oxidative Stress/drug effects ; Rats ; Reproduction/drug effects ; Sperm Count ; Sperm Motility/drug effects ; Testis/injuries ; Testis/metabolism ; Vitamin B Complex/pharmacology
Chemical Substances	Vitamin B Complex (12001-76-2) ; Methotrexate (YL5FZ2Y5U1)
Language	English
Publishing date	2020-10-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2020/4372719
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