We are analyzing https://link.springer.com/article/10.1007/s12011-019-01865-6.

Title:
Diacerein Downregulates NLRP3/Caspase-1/IL-1β and IL-6/STAT3 Pathways of Inflammation and Apoptosis in a Rat Model of Cadmium Testicular Toxicity | Biological Trace Element Research
Description:
The potential gonadal protective effect of diacerein (DCN) and its underlying mechanisms were studied in a rat model of cadmium-induced testicular toxicity. The rats received DCN (50 mg/kg/day, p.o.) for 10 days and one injection of CdCl2 (2 mg/kg, i.p.) on day 9. Cadmium significantly declined serum testosterone and significantly raised interleukin-1β, interleukin-6, interleukin-18, tumor necrosis factor-α, caspase-1, phosphorylated signal transducer and activator of transcription-3 (pSTAT3), nuclear factor-κB p65, Bax, and caspase-3 in rat testes. DCN significantly ameliorated the changes in the biochemical measurements observed with CdCl2 insult. Additionally, DCN preserved the normal testicular architecture, maintained spermatogenesis, and lowered the expression of NOD-like receptor family protein 3 (NLRP3) inflammasome in testes of rats that received CdCl2. It was concluded that DCN significantly protected the gonads of male rats exposed to cadmium toxicity through modulation of NLRP3/caspase-1/IL-1β and IL-6/STAT3 pathways of inflammation and apoptosis.
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Keywords {🔍}

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Topics {✒️}

diacerein downregulates nlrp3/caspase-1/il-1β nlrp3/caspase-1/il-1β ischemia-reperfusion-induced testicular injury ameliorating cadmium-induced testes-toxicity cadmium induced-stat3 activation significantly raised interleukin-1β cadmium chloride-induced toxicity month download article/chapter dss-induced ulcerative colitis cadmium-induced testicular toxicity nuclear factor-κb p65 pi3k/akt/nrf-2 signaling tumor necrosis factor-α inhibiting tlr4/nf-κb inhibiting cadmium-induced apoptosis il-6/stat3 pathways endoplasmic reticulum stress research ethics committee doxorubicin-induced nephrotoxicity full article pdf cadmium testicular toxicity nlrp3 inflammasome privacy choices/manage cookies socs3/stat3 pathway acute cadmium exposure lung cell proliferation nf-κb downregulation normal testicular architecture vascular endothelial cells abdel moneim ae downstream signaling proteins additional information publisher modulating oxidative stress increase disease tolerance osteoarthritis disease process dcn significantly ameliorated dcn significantly protected european economic area phosphorylated signal transducer biochemical measurements observed related subjects int/document/e91044 grape seed proanthocyanidins placebo-controlled trial immunohistochemical staining methods dako north america xbp-1s deacetylation gomez-quiroz le gutierrez ruiz mc abdel-aziz & azza

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         description:The potential gonadal protective effect of diacerein (DCN) and its underlying mechanisms were studied in a rat model of cadmium-induced testicular toxicity. The rats received DCN (50 mg/kg/day, p.o.) for 10 days and one injection of CdCl2 (2 mg/kg, i.p.) on day 9. Cadmium significantly declined serum testosterone and significantly raised interleukin-1β, interleukin-6, interleukin-18, tumor necrosis factor-α, caspase-1, phosphorylated signal transducer and activator of transcription-3 (pSTAT3), nuclear factor-κB p65, Bax, and caspase-3 in rat testes. DCN significantly ameliorated the changes in the biochemical measurements observed with CdCl2 insult. Additionally, DCN preserved the normal testicular architecture, maintained spermatogenesis, and lowered the expression of NOD-like receptor family protein 3 (NLRP3) inflammasome in testes of rats that received CdCl2. It was concluded that DCN significantly protected the gonads of male rats exposed to cadmium toxicity through modulation of NLRP3/caspase-1/IL-1β and IL-6/STAT3 pathways of inflammation and apoptosis.
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      description:The potential gonadal protective effect of diacerein (DCN) and its underlying mechanisms were studied in a rat model of cadmium-induced testicular toxicity. The rats received DCN (50 mg/kg/day, p.o.) for 10 days and one injection of CdCl2 (2 mg/kg, i.p.) on day 9. Cadmium significantly declined serum testosterone and significantly raised interleukin-1β, interleukin-6, interleukin-18, tumor necrosis factor-α, caspase-1, phosphorylated signal transducer and activator of transcription-3 (pSTAT3), nuclear factor-κB p65, Bax, and caspase-3 in rat testes. DCN significantly ameliorated the changes in the biochemical measurements observed with CdCl2 insult. Additionally, DCN preserved the normal testicular architecture, maintained spermatogenesis, and lowered the expression of NOD-like receptor family protein 3 (NLRP3) inflammasome in testes of rats that received CdCl2. It was concluded that DCN significantly protected the gonads of male rats exposed to cadmium toxicity through modulation of NLRP3/caspase-1/IL-1β and IL-6/STAT3 pathways of inflammation and apoptosis.
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