Effect of a derivatized tetrapeptide from lactoferrin on nitric oxide mediated matrix metalloproteinase-2 production by synovial fibroblasts in collagen-induced arthritis in rats

Kumar, Dilly Ashok; Raju, K. Venkateswara; Settu, Kandakumar; Kumanan, K.; Puvanakrishnan, Rengarajulu

doi:10.1016/j.peptides.2005.11.001

Cited by 8 publications

(6 citation statements)

References 36 publications

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“…14,18 On the other hand, MTX increased ROS production in the kidneys and liver, possibly damaging them. 3,4 Reactive oxygen species stimulates chondrocytes and synovial fi broblasts to secrete matrix-metalloproteinases 20 and causes synovitis and destruction of the joints of RA. 7,8,21,22 H 2 O 2 and superoxide (O 2 −) has been shown to accelerate bone resorption by osteoclasts.…”

Section: Discussionmentioning

confidence: 99%

Methotrexate reduces the levels of pentosidine and 8-hydroxy-deoxy guanosine in patients with rheumatoid arthritis

et al. 2007

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This study was performed to investigate whether methotrexate (MTX) affects the levels of oxidative stress markers, including pentosidine one of the glycation end products (AGEs) or 8-hydroxy-deoxy guanosine (8-OHdG). These stress markers represent DNA damage; 19 rheumatoid arthritis (RA) patients underwent MTX treatment. The levels of serum total, urinary total, urinary-free pentosidine and also urinary 8-OHdG, as well as clinical parameters, including disease activity scores for 28 joints (DAS28) were measured at baseline and at 3 and 6 months after the initial treatment with MTX. After the initial treatment with MTX, serum total and urinary total pentosidine levels were reduced at 6 months, and urinary-free pentosidine levels were reduced at 3 and 6 months. Urinary 8-OHdG levels also were significantly reduced at 6 months after the initial treatment with MTX. This study demonstrated that MTX plays a role as a regulator against pentosidine formation and oxidative DNA damage in RA patients.

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Section: Discussionmentioning

confidence: 99%

Methotrexate reduces the levels of pentosidine and 8-hydroxy-deoxy guanosine in patients with rheumatoid arthritis

et al. 2007

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“…Proinflammatory cytokines and microorganism-derived degradation products stimulate the activation of different transcription factors involved in the transcriptional regulation of several genes, including iNOS. To this regard, rheumatoid arthritis (RA) and osteoarthritis (OA) are both welldocumented examples in which high levels of NO contribute to tissue destruction by increasing MMP expression [89,90,91], and up-regulation of p53 [92] and Akt phosphorylation[93]-mediated apoptosis [94]. Further destruction of the tissue is associated with enhanced production of NO in peripheral blood mononuclear cells [95] and NO-mediated abnormal T-cell accumulation in the joints of patients with RA [96,97].…”

Section: Nitric Oxide and Diseasementioning

confidence: 99%

Recent Insights into the Implication of Nitric Oxide in Osteoblast Differentiation and Proliferation during Bone Development

Saura

Tarin²,

Zaragoza³

2010

The Scientific World JOURNAL

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Bone tissue renovation is a dynamic event in which osteoblasts and osteoclasts are responsible for the turnover between bone formation and bone resorption, respectively. During bone development, extracellular matrix remodeling is required for osteoblast differentiation and the process is largely mediated by the proteolytic activity of extracellular matrix metalloproteinases (MMPs), which play a fundamental role in osteoblast migration, unmineralized matrix degradation, and cell invasion. The recent advances towards investigation in osteogenesis have provided significant information about the transcriptional regulation of several genes, including MMPs, by the expression of crucial transcription factors like NFAT, ATF4, osterix, TAZ, and Cbfa-1–responsive elements. Evidence from gene knock-out studies have shown that bone formation is, at least in part, mediated by nitric oxide (NO), since mice deficient in endothelial nitric oxide synthase (eNOS) and mice deficient in the eNOS downstream effector (cGMP)-dependent protein kinase (PKG) show bone abnormalities, while inducible NOS (iNOS) null mice also show imbalances in bone osteogenesis and abnormalities in bone healing. Recently, in vitro data showed that Cbfa-1 and the MAPK pathways were crucial for osteoblastic cell differentiation, and NO was found to play a significant role. This article sheds light on some of the mechanisms that may influence NO-mediated actions in bone development.

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“…The study was conducted on male Wistar rats, weighing 225-250 g. They were housed in individual cages under standard environmental conditions (24 ± 1 o C on a 12-hour light/ dark cycle) (Kumar et al, 2005) and maintained with free access to standard laboratory rat food pellets and water ad libitum. Then animals were divided into three groups, each group containing 10 animals (n = 10 per groups).…”

Section: Animalsmentioning

confidence: 99%

Dexamethasone Release from Glutaraldehyde Cross-Linked Chitosan Microspheres: In Vitro/In Vivo Studies and Non-Clinical Parameters Response in Rat Arthritic Model

Dhanaraju¹,

Elizabeth²,

Ganesan³

2011

Journal of Pharmaceutical Investigation

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− The Dexamethasone (DEX) loaded chitosan microspheres were prepared by thermal denaturation and chemical cross-linking method using a dierent concentration of glutaraldehyde as chemical cross-linking agent. The prepared microspheres were evaluated for the percentage of Drug Loading (DL), Encapsulation Efficiency (EE) and surface morphology by Scanning Electron Microscopy (SEM). DL and EE were found to be maximum range of 10.0 to 10.79 % and 58.19 to 64.73 % respectively. The SEM Photographs of the resultant microspheres exhibited fairly smooth surfaces and predominantly spherical in appearance. In addition, Fourier Transform Infrared Spectroscopy (FTIR) and Differential Scanning Calorimetry (DSC) shown that there was no interaction between the drug and polymer. In vitro and in vivo release studies revealed that the release of dexamethasone was sustained and extended up to 63 days and effectively controlled by the extent of cross-linking agent. Non-clinical parameters such as paw volume, hematological parameters like Erythrocyte Sedimentation Rate (ESR), Paced Cell Volume (PCV), Total Leucocytes Count (TLC), Hemoglobin (Hb), Differential Cell Count (DCC) were investigated in Fruend's Complete Adjuvant (FCA) induced arthritic rats. Radiology and histopathological studies were also performed in order to evaluate the therapeutic efficacy of the DEX-loaded microspheres in extenuating the rat arthritic model.

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Effect of a derivatized tetrapeptide from lactoferrin on nitric oxide mediated matrix metalloproteinase-2 production by synovial fibroblasts in collagen-induced arthritis in rats

Cited by 8 publications

References 36 publications

Methotrexate reduces the levels of pentosidine and 8-hydroxy-deoxy guanosine in patients with rheumatoid arthritis

Methotrexate reduces the levels of pentosidine and 8-hydroxy-deoxy guanosine in patients with rheumatoid arthritis

Recent Insights into the Implication of Nitric Oxide in Osteoblast Differentiation and Proliferation during Bone Development

Dexamethasone Release from Glutaraldehyde Cross-Linked Chitosan Microspheres: In Vitro/In Vivo Studies and Non-Clinical Parameters Response in Rat Arthritic Model

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