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      Salidroside ameliorates arthritis-induced brain cognition deficits by regulating Rho/ROCK/NF-κB pathway.

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          Abstract

          The prevalence of cognitive impairment in rheumatoid arthritis (RA) patients was increasingly serious nowadays. The purpose of the current study was to explore whether salidroside (Sal) could alleviate arthritis-induced cognition deficits and examine the relationship between the impairment and Rho/ROCK/NF-κB pathway. Collagen-induced arthritis (CIA) was established by the injection of chicken type II collagen (CII), complete Freund's adjuvant (CFA) and incomplete Freund's adjuvant (IFA). Arthritic lesions of CIA rats were assessed by arthritis index score, swelling of paws and histological analysis. Cognitive deficits symptoms of CIA rats were monitored through Morris water maze test. The contents of pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) in hippocampus and serum were significantly reduced with salidroside (20 mg/kg, 40 mg/kg) treatment compared with those in the CIA group. In parallel, we demonstrated that the expressions of RhoA, ROCK1, ROCK2, p-NF-κBp65, p-IκBα, p-IKKα and p-IKKβ were enhanced accompanying the investigation arthritis-induced cognition deficits, which were remarkably down-regulated by salidroside and confirmed by the results obtained from western blot and immunohistochemistry. LC-MS/MS results ascertained that Sal could enter into the blood and brain tissues to exhibit the protective effect on arthritis-induced cognitive dysfunction. Therefore, it was assumed that Sal might be a potential therapeutic candidate to treat arthritis-induced brain cognition deficits through the regulation of Rho/ROCK/NF-κB signaling.

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          Author and article information

          Journal
          Neuropharmacology
          Neuropharmacology
          Elsevier BV
          1873-7064
          0028-3908
          Apr 2016
          : 103
          Affiliations
          [1 ] Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China; Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China.
          [2 ] State Key Laboratory of Natural Medicines, Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China.
          [3 ] Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China.
          [4 ] Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China.
          [5 ] School of Engineering, China Pharmaceutical University, Nanjing 210009, China.
          [6 ] Nanjing Municipal Hospital of T.C.M, The Third Affiliated Hospital of Nanjing University of T.C.M, Nanjing 210001, China. Electronic address: hongyan3128@163.com.
          [7 ] Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: liuyuyaoda@163.com.
          [8 ] Department of Biochemistry, School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, China; Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: yantianhuabest@126.com.
          [9 ] Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: machunhuabest@126.com.
          Article
          S0028-3908(15)30203-3
          10.1016/j.neuropharm.2015.12.007
          26690894
          73ff36cc-a3d0-4204-be17-667fc2a8b0af
          History

          Brain cognition deficits,Inflammation,Rho/ROCK/NF-κB,Salidroside,Arthritis

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