Glucosamine prevents in vitro collagen degradation in chondrocytes by inhibiting advanced lipoxidation reactions and protein oxidation

Osteoarthritis (OA) affects a large segment of the aging population and is a major cause of pain and disability. At present, there is no specific treatment available to prevent or retard the cartilage destruction that occurs in OA. Recently, glucosamine sulfate has received attention as a putative agent that may retard cartilage degradation in OA. The precise mechanism of action of glucosamine is not known. We investigated the effect of glucosamine in an in vitro model of cartilage collagen degradation in which collagen degradation induced by activated chondrocytes is mediated by lipid peroxidation reaction. Lipid peroxidation in chondrocytes was measured by conjugated diene formation. Protein oxidation and aldehydic adduct formation were studied by immunoblot assays. Antioxidant effect of glucosamine was also tested on malondialdehyde (thiobarbituric acid-reactive substances [TBARS]) formation on purified lipoprotein oxidation for comparison. Glucosamine sulfate and glucosamine hydrochloride in millimolar (0.1 to 50) concentrations specifically and significantly inhibited collagen degradation induced by calcium ionophore-activated chondrocytes. Glucosamine hydrochloride did not inhibit lipid peroxidation reaction in either activated chondrocytes or in copper-induced oxidation of purified lipoproteins as measured by conjugated diene formation. Glucosamine hydrochloride, in a dose-dependent manner, inhibited malondialdehyde (TBARS) formation by oxidized lipoproteins. Moreover, we show that glucosamine hydrochloride prevents lipoprotein protein oxidation and inhibits malondialdehyde adduct formation in chondrocyte cell matrix, suggesting that it inhibits advanced lipoxidation reactions. Together, the data suggest that the mechanism of decreasing collagen degradation in this in vitro model system by glucosamine may be mediated by the inhibition of advanced lipoxidation reaction, preventing the oxidation and loss of collagen matrix from labeled chondrocyte matrix. Further studies are needed to relate these in vitro findings to the retardation of cartilage degradation reported in OA trials investigating glucosamine

Cervical Spondylotic Myelopathy: Factors in Choosing the Surgical Approach

Cervical spondylotic myelopathy is a progressive disease and a common cause of acquired disability in the elderly. A variety of surgical interventions are available to halt or improve progression of the disease. Surgical options include anterior or posterior approaches with and without fusion. These include anterior cervical discectomy and fusion, anterior cervical corpectomy and fusion, cervical disc replacement, laminoplasty, laminectomy with and without fusion, and combined approaches. Recent investigation into the ideal approach has not found a clearly superior choice, but individual patient characteristics can guide treatment

Glucosamine hydrochloride does not prevent conjugated diene formation by calcium ionophore-stimulated chondrocytes or by copper-catalyzed oxidation of low-density lipoprotein

<p><b>Copyright information:</b></p><p>Taken from "Glucosamine prevents collagen degradation in chondrocytes by inhibiting advanced lipoxidation reactions and protein oxidation"</p><p>http://arthritis-research.com/content/9/4/R76</p><p>Arthritis Research & Therapy 2007;9(4):R76-R76.</p><p>Published online 8 Aug 2007</p><p>PMCID:PMC2206377.</p><p></p> A washed monolayer of primary articular chondrocytes in 60-mm Petri dishes was stimulated in the presence or absence of A23187 (20 μm) with or without glucosamine (50 mM) or Vitamin E (250 μM) in phenol-free Earl's balanced salt solution. The media were monitored for conjugated diene formation at 234 nm at different time points. Delta absorbance shown is absorbance at different time points minus the absorbance at 0 hours. A representative of four experiments is shown. Low-density lipoprotein (0.25 mg/ml) was incubated at 30°C in phosphate-buffered saline alone (open circles) or in the presence of 5 μM Cu(closed circles) or with 5 μM Cuand 25 mM (open triangles) or 0.25 mM (closed triangles) glucosamine. A conjugated diene formation was monitored at 234 nm. Ca Iono, calcium ionophore; Cu, copper; Glu, glucosamine; LDL, low-density lipoprotein; Vit E, vitamin E

Glucosamine hydrochloride inhibits malondialdehyde formation by lipoprotein oxidation

<p><b>Copyright information:</b></p><p>Taken from "Glucosamine prevents collagen degradation in chondrocytes by inhibiting advanced lipoxidation reactions and protein oxidation"</p><p>http://arthritis-research.com/content/9/4/R76</p><p>Arthritis Research & Therapy 2007;9(4):R76-R76.</p><p>Published online 8 Aug 2007</p><p>PMCID:PMC2206377.</p><p></p> Lipoproteins (0.5 mg/ml) were incubated at 30°C in phosphate-buffered saline for 4 hours in the absence or presence of 5 μM Cuor 5 μM Cuand 50, 5, or 0.5 mM glucosamine hydrochloride. Data are expressed as malondialdehyde equivalents in nanomoles and are presented as the mean of a duplicate set of samples ± standard error. A representative of two experiments is shown. Cu, copper; Glu, glucosamine hydrochloride; LDL, low-density lipoprotein

Effect of glucosamine-derived compounds on calcium ionophore-induced release of H-proline-labeled articular collagen matrix

<p><b>Copyright information:</b></p><p>Taken from "Glucosamine prevents collagen degradation in chondrocytes by inhibiting advanced lipoxidation reactions and protein oxidation"</p><p>http://arthritis-research.com/content/9/4/R76</p><p>Arthritis Research & Therapy 2007;9(4):R76-R76.</p><p>Published online 8 Aug 2007</p><p>PMCID:PMC2206377.</p><p></p> [H]-proline-labeled monolayer of primary articular chondrocytes in 24-well plates was stimulated with calcium ionophore A23187 (15 μM) in the presence or absence of glucosamine hydrochloride (Glu) (25 mM), glucosamine sulfate (GS) (25 mM), -acetyl glucosamine (N-A Glu) (25 mM), and -acetyl mannosamine (N-A Mann) (25 mM). The 4-hour percentage release of labeled matrix collagen is shown. The results are presented as the mean of triplicate sets of wells ± standard error. A representative of three experiments is shown. *Statistically significant between cells stimulated with calcium ionophore and with Glu or GS. Ca Iono, calcium ionophore

Seronegative Atypical Anti-Glomerular Basement Membrane Glomerulonephritis Associated With Thrombotic Microangiopathy: Case Report and Literature Analysis

Anti-glomerular basement membrane (GBM) antibody nephritis is defined by linear immunofluorescence staining of GBM by immunoglobulin G (IgG), typically associated with GBM rupture, fibrinoid necrosis, and crescent formation. Clinically, the patients present with rapidly worsening renal function, often with hematuria. Typical renal pathologic findings include necrotizing and crescentic glomerulonephritis. In contrast, thrombotic microangiopathy (TMA) is characterized by microvascular thrombosis, which can also lead to acute kidney injury. Thrombotic microangiopathy is associated with some systemic diseases and has characteristic clinical features of microangiopathic hemolytic anemia, platelet consumption, and multiple organ failure. Anti-GBM nephritis associated with TMA has rarely been reported. We describe an unusual case of atypical anti-GBM disease without crescent formation or necrosis but with light microscopic and ultrastructural features consistent with endothelial cell injury and glomerular-limited TMA