RETRACTED ARTICLE: Silibinin ameliorates arsenic induced nephrotoxicity by abrogation of oxidative stress, inflammation and apoptosis in rats
Authors: S Milton Prabu
M Muthumani
Journal: Molecular Biology Reports (2012)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Arsenic; Silibinin; Kidney toxicity; Antioxidants; Nephroprotective
Affiliations: Department of Zoology, Faculty of Science, Annamalai University, Annamalainagar, 608 002, Tamil Nadu, India. 

Abstract:  Arsenic (As) is an environmental and industrial pollutant that affects various organs in human and experimental animals. Silibinin is a naturally occurring plant bioflavonoid found in the milk thistle of Silybum marianum, which has been reported to have a wide range of pharmacological properties. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of As toxicity. Since kidney is the critical target organ of chronic As toxicity, we carried out this study to investigate the effects of silibinin on As-induced toxicity in the kidney of rats. In experimental rats, oral administration of sodium arsenite [NaAsO(2), 5 mg/(kg day)] for 4 weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid, creatinine with a significant (p &lt; 0.05) decrease in creatinine clearance. As also significantly decreased the levels of urea, uric acid and creatinine in urine. A markedly increased levels of lipid peroxidation markers (thiobarbituric acid reactive substances and lipid hydroperoxides) and protein carbonyl contents with significant (p &lt; 0.05) decrease in non-enzymatic antioxidants (total sulfhydryl groups, reduced glutathione, vitamin C and vitamin E) and enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase), Glutathione metabolizing enzymes (glutathione reductase and glutathione-6-phosphate dehydrogenase) and membrane bound ATPases were also observed in As treated rats. Co-administration of silibinin (75 mg/kg day) along with As resulted in a reversal of As-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. The histopathological and immunohistochemical studies in the kidney of rats also shows that silibinin (75 mg/kg day) markedly reduced the toxicity of As and preserved the normal histological architecture of the renal tissue, inhibited the caspase-3 mediated tubular cell apoptosis and decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue. The present study suggests that the nephroprotective potential of silibinin in As toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in As-induced renal damage. 

Retracted: Yes

PubPeer comments:
 ![file] * This preformation was carried out under the manufacturers with some changes. In brief, the tendon cells of logical germination phage were collected and seeded into 96 well plates at the destiny of $10^6$ cells each well. **From whom** were the cells harvested? And based on which ethics approval? The paper says nothing... **Logical growth** is a *tortured phrase* used in lieu of *logarithmic growth*. This is one hallmark of a [prolific coordination polymer papermill] . ![file] Another typical sign of the mentioned papermill is a curious plot with quasi-logarithmic scale on the x-axis, with a larger-than-one-may-expect jump of value between 8 and 10 units. , 
 Table 1 indicates that the crystallography results were deposited in the CCDC database as entries 1991201 and 1991200. ![file] The database informs us that the crystallographer associated with these entries was  haitao Yuan , of Bohai University. No-one of that name is credited anywhere in the paper. Haitao Yuan was industrious during 2020, uploading [**134** crystallography reports to the database] . 17 of these became the foundations of various papers by unrelated authors, leaving another 117 to become the foundations of future papers. , 
 *[left]* Fig 9,  Inhibited activation of the FAK signaling route in the tendon cells after compound treatment. *[right]* Fig 7 from [Li et al (2020)] ,  Inhibited NF-kB signaling pathway activation in macrophages after treated by compound . ![file] The GAPDH loading bands are surprisingly similar apart from exposure level. Here is an attempt to match the lightness: ![file] ,