N-(2-hydroxy phenyl) acetamide inhibits inflammation-related cytokines and ROS in adjuvant-induced arthritic (AIA) rats

Jawed, Huma; Shah, Syed Muhammad Hassan; Jamall, Siddiqua; Simjee, Shabana Usman

doi:10.1016/j.intimp.2010.04.028

Cited by 54 publications

(33 citation statements)

References 57 publications

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“…The mechanisms underlying cartilage destruction are numerous and interrelated. These include the involvement of ROS, NO and several cytokines (Arend 2001, Henrotin et al 2003, Jawed et al 2010). This was confirmed in the present study, where the induction of arthritis resulted in a reduction in the level of reduced glutathione associated with a corresponding rise in MDA (oxidative stress parameters) and a rise in the level of NO in the serum.…”

Section: Discussionmentioning

confidence: 99%

The influence of irradiation on the potential chondroprotective effect of aqueous extract of propolis in rats

El‐Ghazaly

el-naby

Khayyal

2010

International Journal of Radiation Biology

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Section: Discussionmentioning

confidence: 99%

The influence of irradiation on the potential chondroprotective effect of aqueous extract of propolis in rats

El‐Ghazaly

el-naby

Khayyal

2010

International Journal of Radiation Biology

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“…However, N -carbamylglutamate decreased urinary acetamide. Acetamide exhibits anti-microbial, anti-inflammatory, anti-arthritic, and antibiotic functions [36,37]. Changes in these metabolites are attributed to the altered activity of intestinal microorganisms.…”

Section: Discussionmentioning

confidence: 99%

Urinary Metabolomic Approach Provides New Insights into Distinct Metabolic Profiles of Glutamine and N-Carbamylglutamate Supplementation in Rats

et al. 2016

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Glutamine and N-carbamylglutamate can enhance growth performance and health in animals, but the underlying mechanisms are not yet elucidated. This study aimed to investigate the effect of glutamine and N-carbamylglutamate supplementation in rat metabolism. Thirty rats were fed a control, glutamine, or N-carbamylglutamate diet for four weeks. Urine samples were analyzed by nuclear magnetic resonance (NMR)-based metabolomics, specifically high-resolution 1H NMR metabolic profiling combined with multivariate data analysis. Glutamine significantly increased the urine levels of acetamide, acetate, citrulline, creatinine, and methymalonate, and decreased the urine levels of ethanol and formate (p < 0.05). Moreover, N-carbamylglutamate significantly increased the urine levels of creatinine, ethanol, indoxyl sulfate, lactate, methymalonate, acetoacetate, m-hydroxyphenylacetate, and sarcosine, and decreased the urine levels of acetamide, acetate, citrulline, creatine, glycine, hippurate, homogentisate, N-acetylglutamate, phenylacetyglycine, acetone, and p-hydroxyphenylacetate (p < 0.05). Results suggested that glutamine and N-carbamylglutamate could modify urinary metabolome related to nitrogen metabolism and gut microbiota metabolism. Moreover, N-carbamylglutamate could alter energy and lipid metabolism. These findings indicate that different arginine precursors may lead to differences in the biofluid profile in rats.

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“…Induction of AIA and administration of NOR Experimental arthritis was induced by an intradermal injection with 0.1 mL of 10 mg/mL Mycobacterium butyricum in Freund's complete adjuvant at the base of the right hind paw and the tail of the rats [12][13][14] . On d 14 after immunization, rats were assigned randomly to one of the following six groups: the normal group (treatment with 0.5% CMC-Na, the vehicle), the model group (treatment with 0.5% CMC-Na, the vehicle), three NOR groups (treatment with 7.5, 15, and 30 mg/kg) and the DEX group (treatment with 0.5 mg/kg).…”

Section: Animalsmentioning

confidence: 99%

Norisoboldine alleviates joint destruction in rats with adjuvant-induced arthritis by reducing RANKL, IL-6, PGE2, and MMP-13 expression

et al. 2013

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Aim: To explore the effects of norisoboldine (NOR), a major isoquinoline alkaloid in Radix Linderae, on joint destruction in rats with adjuvant-induced arthritis (AIA) and its underlying mechanisms. Methods: AIA was induced in adult male SD rats by intradermal injection of Mycobacterium butyricum in Freund's complete adjuvant at the base of the right hind paw and tail. From d 14 after immunization, the rats were orally given NOR (7.5, 15, or 30 mg/kg) or dexamethasone (0.5 mg/kg) daily for 10 consecutive days. Joint destruction was evaluated with radiological scanning and H&E staining. Fibroblast-like synoviocytes (FLS) were prepared from fresh synovial tissues in the AIA rats. The expression of related proteins and mRNAs were detected by ELISA, Western blotting and RT-PCR. Results: In AIA rats, NOR (15 and 30 mg/kg) significantly decreased the swelling of paws and arthritis index scores, and elevated the mean body weight. NOR (30 mg/kg) prevented both the infiltration of inflammatory cells and destruction of bone and cartilage in joints. However, NOR (15 mg/kg) only suppressed the destruction of bone and cartilage, but did not obviously ameliorate synovial inflammation. NOR (15 and 30 mg/kg) significantly decreased the serum levels of receptor activator of nuclear factor κB ligand (RANKL), IL-6, PGE 2 , and MMP-13, but not the osteoprotegerin and MMP-1 levels. The mRNA levels of RANKL, IL-6, COX-2, and MMP-13 in synovium were also suppressed. Dexamethasone produced similar effects in AIA rats as NOR did, but without elevating the mean body weight. In the cultured FLS, treatment with NOR (10 and 30 mmol/L) significantly decreased the secretion of RANKL, IL-6, PGE 2 , and MMP-13 proteins. Furthermore, the treatment selectively prevented the activation of MAPKs, AKT and transcription factor AP-1 component c-Jun, but not the recruitment of TRAF6 or the activation of JAK2/STAT3. Treatment of the cultured FLS with the specific inhibitors of p38, ERK, AKT, and AP-1 significantly decreased the secretion of RANKL, IL-6, PGE 2 , and MMP-13 proteins. Conclusion: NOR can alleviate joint destruction in AIA rats by reducing RANKL, IL-6, PGE 2 , and MMP-13 expression via the p38/ERK/ AKT/AP-1 pathway.

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N-(2-hydroxy phenyl) acetamide inhibits inflammation-related cytokines and ROS in adjuvant-induced arthritic (AIA) rats

Cited by 54 publications

References 57 publications

The influence of irradiation on the potential chondroprotective effect of aqueous extract of propolis in rats

The influence of irradiation on the potential chondroprotective effect of aqueous extract of propolis in rats

Urinary Metabolomic Approach Provides New Insights into Distinct Metabolic Profiles of Glutamine and N-Carbamylglutamate Supplementation in Rats

Norisoboldine alleviates joint destruction in rats with adjuvant-induced arthritis by reducing RANKL, IL-6, PGE2, and MMP-13 expression

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