Protective effects of natural products against drug-induced nephrotoxicity: a review in recent years

2021 ◽  
pp. 112255
Author(s):  
Chen Gao ◽  
Chang Liu ◽  
Yuwei Chen ◽  
Qingtao Wang ◽  
Zhihui Hao
Keyword(s):  
Natural Products ◽  
Protective Effects ◽  
Drug Induced

A review of the potential protective effects of pentoxifylline against drug-induced nephrotoxicity

2012 ◽  
Vol 69 (5) ◽  
pp. 1057-1073 ◽  
Author(s):  
Zahra Nasiri-Toosi ◽  
Simin Dashti-Khavidaki ◽  
Hossein Khalili ◽  
Mahboob Lessan-Pezeshki
Keyword(s):  
Protective Effects ◽  
Drug Induced

scholarly journals Hepatoprotective effects of Sapium sebiferum in paracetamol-induced liver injury

2015 ◽  
Vol 10 (2) ◽  
pp. 393 ◽  
Author(s):  
Liaqat Hussain ◽  
Muhammad Sajid Hamid Akash ◽  
Madeha Tahir ◽  
Kanwal Rehman
Keyword(s):  
Liver Injury ◽  
Serum Levels ◽  
Therapeutic Effects ◽  
Sapium Sebiferum ◽  
Dependent Manner ◽  
Protective Effects ◽  
Drug Induced ◽  
Standard Drug ◽  
Hepatoprotective Effects ◽  
Dose Dependent

<span><em>Sapium sebiferum</em> leaves were used to determine its hepatoprotective effects against paracetamol-induced hepatotoxicity in mice. A dose dependent study was conducted using two different doses (200 mg/kg and 400 mg/kg) of the extract of </span><em>S. sebiferum</em><span> against toxic effects of paracetamol (500 mg/kg) in experimental animal model. Silymarin (50 mg/kg) was used as standard drug to compare therapeutic effects of </span><em>S. sebiferum</em><span> with control and paracetamol-treated groups. Paracetamol significantly increased the serum levels of liver enzyme markers like alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bilirubin, and direct bilirubin. The extract showed protective effects by normalizing the liver enzymes markers in a dose dependent manner. Histopathological results confirmed the hepatoprotective effects of leaves of </span><em>S. sebiferum</em><span>. We conclude that leaves of </span><em>S. sebiferum</em><span> have strong hepatoprotective effects against paracetamol-induced liver injury and can be used in liver injuries caused by drug-induced toxicity.</span>

Ginsenoside Rb1, A Major Saponin from Panax ginseng, Exerts Protective Effects Against Acetaminophen-Induced Hepatotoxicity in Mice

2019 ◽  
Vol 47 (08) ◽  
pp. 1815-1831 ◽  
Author(s):  
Shen Ren ◽  
Jing Leng ◽  
Xing-Yue Xu ◽  
Shuang Jiang ◽  
Ying-Ping Wang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Panax Ginseng ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Protective Effects ◽  
Ginsenoside Rb1 ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Oxide Synthase

Acute liver injury (ALI) induced by acetaminophen (APAP) is the main cause of drug-induced liver injury. Previous reports indicated liver failure could be alleviated by saponins (ginsenosides) from Panax ginseng against APAP-induced inflammatory responses in vivo. However, validation towards ginsenoside Rb1 as a major and marker saponin may protect liver from APAP-induced ALI and its mechanisms are poorly elucidated. In this study, the protective effects and the latent mechanisms of Rb1 action against APAP-induced hepatotoxicity were investigated. Rb1 was administered orally with 10[Formula: see text]mg/kg and 20[Formula: see text]mg/kg daily for 1 week before a single injection of APAP (250[Formula: see text]mg/kg, i.p.) 1[Formula: see text]h after the last treatment of Rb1. Serum alanine/aspartate aminotransferases (ALT/AST), liver glutathione (GSH) depletion, as well as the inflammatory cytokines, such as tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1[Formula: see text] (IL-1[Formula: see text]), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), were analyzed to indicate the underlying protective effects of Rb1 against APAP-induced hepatotoxicity with significant inflammatory responses. Histological examination further proved Rb1’s protective effects. Importantly, Rb1 mitigated the changes in the phosphorylation of MAPK and PI3K/Akt, as well as its downstream factor NF-[Formula: see text]B. In conclusion, experimental data clearly demonstrated that Rb1 exhibited a remarkable liver protective effect against APAP-induced ALI, partly through regulating MAPK and PI3K/Akt signaling pathways-mediated inflammatory responses.

Pyridoxine and GABA as antagonists to drug-induced convulsions in monkeys

1965 ◽  
Vol 20 (6) ◽  
pp. 1337-1340 ◽  
Author(s):  
Lenore M. Kopeloff ◽  
Joseph G. Chusid
Keyword(s):  
Macaca Mulatta ◽  
Vitamin B6 ◽  
Aminobutyric Acid ◽  
Experimental Epilepsy ◽  
Protective Effects ◽  
Gamma Aminobutyric Acid ◽  
Drug Induced

The antagonistic properties of pyridoxine and gamma aminobutyric acid (GABA) toward convulsant drugs were evaluated by determining their in vivo protective effects when administered parenterally prior to challenge. In a group of 28 monkeys composed of 19 chronic epileptics and 9 controls, pyridoxine and GABA provided variable grades of protection against the convulsant actions of methoxypyridoxine, semicarbazide, and to a lesser degree, pentamethylenetetrazol (Metrazol) and 3,3-methylethylglutarimide (Megimide). Neither pyridoxine nor GABA protected epileptic, brain-operated nonepileptic, or normal monkeys from the convulsant actions of parenteral picrotoxin. No evidence therefore was found in these experiments to support the suggestion that GABA (or pyridoxine) and picrotoxin are antagonistic to each other. experimental epilepsy in Macaca mulatta; gamma aminobutyric acid and vitamin B6 as anticonvulsants Submitted on February 15, 1965

scholarly journals Antioxidant Supplementation in the Treatment of Neurotoxicity Induced by Platinum-Based Chemotherapeutics—A Review

2020 ◽  
Vol 21 (20) ◽  
pp. 7753
Author(s):  
Jelena S. Katanic Stankovic ◽  
Dragica Selakovic ◽  
Vladimir Mihailovic ◽  
Gvozden Rosic
Keyword(s):  
Ros Generation ◽  
Protective Effects ◽  
Therapeutic Approaches ◽  
Platinum Drug ◽  
Drug Induced ◽  
Root Cause ◽  
Antioxidant Agents ◽  
Plant Antioxidants ◽  
The Many

Cancer represents one of the most pernicious public health problems with a high mortality rate among patients worldwide. Chemotherapy is one of the major therapeutic approaches for the treatment of various malignancies. Platinum-based drugs (cisplatin, oxaliplatin, carboplatin, etc.) are highly effective chemotherapeutic drugs used for the treatment of several types of malignancies, but their application and dosage are limited by their toxic effects on various systems, including neurotoxicity. Simultaneously, researchers have tried to improve the survival rate and quality of life of cancer patients and decrease the toxicity of platinum-containing drugs by combining them with non-chemotherapy-based drugs, dietary supplements and/or antioxidants. Additionally, recent studies have shown that the root cause for the many side effects of platinum chemotherapeutics involves the production of reactive oxygen species (ROS) in naive cells. Therefore, suppression of ROS generation and their inactivation with antioxidants represents an appropriate approach for platinum drug-induced toxicities. The aim of this paper is to present an updated review of the protective effects of different antioxidant agents (vitamins, dietary antioxidants and supplements, medicaments, medicinal plants and their bioactive compounds) against the neurotoxicity induced by platinum-based chemotherapeutics. This review highlights the high potential of plant antioxidants as adjuvant strategies in chemotherapy with platinum drugs.

scholarly journals Mitochondria-Targeted Antioxidants for Treatment of Hearing Loss: A Systematic Review

Antioxidants ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 109 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Mitochondrial Gene ◽  
Protective Effects ◽  
Drug Induced ◽  
Age Related ◽  
Cochlear Damage ◽  
Age Related Hearing Loss

Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients.

scholarly journals Treatment of psychosis in prisons and violent recidivism

BJPsych Open ◽  
2015 ◽  
Vol 1 (2) ◽  
pp. 149-157 ◽  
Author(s):  
Artemis Igoumenou ◽  
Constantinos Kallis ◽  
Jeremy Coid
Keyword(s):  
Substance Dependence ◽  
Cox Regression ◽  
Public Health Problem ◽  
Protective Effects ◽  
Drug Induced ◽  
Important Public Health Problem ◽  
Violent Recidivism ◽  
Drug Induced Psychosis ◽  
Improved Accuracy ◽  
Delayed Time

BackgroundViolence among released prisoners with psychosis is an important public health problem. It is unclear whether treatment in prison can influence criminal behaviour subsequent to release.AimsTo investigate whether treatment in prison can delay time to reoffending.MethodOur sample consisted of 1717 adult prisoners in England and Wales convicted of a serious violent or sexual offence. We used Cox regression to investigate the effects of treatment received in prison on associations between mental illness and time to first reconviction following release.ResultsPrisoners with current symptoms of schizophrenia reoffended quicker following release. Nevertheless, treatment with medication significantly delayed time to violence (18% reduction). Treatment for substance dependence delayed violent and non-violent reoffending among prisoners with drug-induced psychosis.ConclusionsIdentifying prisoners with psychosis and administering treatment in prison have important protective effects against reoffending. Repeated screening with improved accuracy in identification is necessary to prevent cases being missed.

scholarly journals Protective effects of cyclodextrins on drug-induced hemolysis in vitro.

1981 ◽  
Vol 4 (2) ◽  
pp. 142-144 ◽  
Author(s):  
KANETO UEKAMA ◽  
TETSUMI IRIE ◽  
MIKI SUNADA ◽  
MASAKI OTAGIRI ◽  
KENICHI TSUBAKI
Keyword(s):  
Protective Effects ◽  
Drug Induced

Death rate of populations of Bact. lactis aerogenes . II. Environmental and other factors influencing the form of the survival curve

1953 ◽  
Vol 141 (902) ◽  
pp. 126-137 ◽  
Keyword(s):  
Survival Curve ◽  
Synthetic Medium ◽  
Low Permeability ◽  
Protective Effects ◽  
Survival Times ◽  
Drug Induced ◽  
Factors Influencing ◽  
Ample Supply ◽  
Test Population ◽  
Overall Resistance

Populations which have been grown with an ample supply of glucose give approximately exponential survival curves at high acidities, adaptive adjustments, revealed in tests at lower concentrations, being apparently suppressed. Shortage of glucose during previous growth favours survival in the test, and changes the distribution of survival times, the decline of the population being initially delayed. Serial subculture of the bacterial strain in a synthetic medium also leads to initial delays. Ageing the culture before preparation of the suspension for test increases the overall resistance, but has little influence on the initial form of the survival curve. The curves for drug-induced filamentous cultures are closely similar to those for normal cultures. Neither low permeability nor co-operative protective effects between different cells seem to be general causes of delayed lethal action. Damage to the cells during preparation of the test population does not explain why the delay is sometimes absent.

Sign in / Sign up

Export Citation Format

Share Document