Hydrated density of chondroitin sulfate preparations

R. A. Milch

doi:10.1007/bf02151541

The birth of proteoglycans: the nature of the link between protein and carbohydrate of a chondroitin sulfate complex from hyaline cartilage

Biochemical Journal ◽

10.1042/bj2007c002 ◽

2007 ◽

pp. c2

Author(s):

Tim E Hardingham

Keyword(s):

Chondroitin Sulfate ◽

Hyaline Cartilage ◽

Sulfate Complex

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Effect of Glycosaminoglycans on Thrombin- and Atroxin-Induced Fibrin Assembly and Structure

Thrombosis and Haemostasis ◽

10.1055/s-0038-1647117 ◽

1989 ◽

Vol 62 (04) ◽

pp. 1057-1061 ◽

Cited By ~ 7

Author(s):

Marcus E Carr ◽

Patrick L Powers

Keyword(s):

Chondroitin Sulfate ◽

Fiber Diameter ◽

Lag Phase ◽

Low Molecular Weight ◽

Fibrin Gels ◽

Fiber Size ◽

Induced Changes ◽

The Impact ◽

Fiber Radius ◽

Turbidity Increase

SummaryThis study was performed to quantitate the impact of several glycosaminoglycans (GAG) on fibrin assembly and structure. Gel formation was monitored as the increase in optical density at 633 nm subsequent to thrombin (2 NIH u/ml) or atroxin (0.10 mg/ml) addition to solutions of buffered fibrinogen (1 mg/ml) or plasma. Gel absorbance was measured as a function of wavelength (400 to 800 nm) and gel fiber diameter and mass/length ratio (μ) were calculated. Chondroitin sulfate A (CSA)shortened the lag phase, enhanced the maximal rate of turbidity increase, and increased the final gel turbidity of fibrin gels formed by thrombin or atroxin. CSA (16 mg/ml) increased fiber μ from 1.3 to 3.1 × 1013 dalton/cm and fiber radius from 6.0 to 8.6 × 10-6 cm in thrombin-induced gels. μ increased from 0.7 to 2.7 × 1013 dalton/cm and fiber radius from 4 to 7.8 × 10-6 cm for atroxin-induced gels. Above 16 mg/ml, CSA caused fibrinogen precipitation in purified solutions but not in plasma. CSA inhibited thrombin-induced plasma clotting of plasma but effects in atroxin-mediated plasma gels paralleled those seen in purified solutions. Chondroitin sulfate B (CSB)-induced changes in fibrin were similar but slightly less dramatic than those seen with CSA. μ increased from 0.9 to 2.0 × 1013 dalton/cm for thrombin-induced fibrin gels and from 0.8 to 2.3 × 1013 dalton/cm for atroxininduced gels. Low molecular weight heparin (Mr = 5100) slowed fibrin assembly and reduced fiber size by 50% in thrombininduced gels. Changes in μ of atroxin-induced gels were much less pronounced (<20%). This study documents pronounced GAGinduced changes in fibrin structure which vary with GAG species and may mediate significant physiologic functions.

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The Gut Microbiota of Rats under Experimental Osteoarthritis and Administration of Chondroitin Sulfate and Probiotic

Mikrobiolohichnyi Zhurnal ◽

10.15407/microbiolj82.06.064 ◽

2020 ◽

Vol 82 (6) ◽

pp. 64-73

Author(s):

O.H. Korotkyi ◽

◽

T.V. Luhovska ◽

T.M. Serhiychuk ◽

K.O. Dvorshchenko ◽

...

Keyword(s):

Gut Microbiota ◽

Chondroitin Sulfate ◽

Joint Inflammation ◽

Degenerative Joint Disease ◽

Joint Disease ◽

Quantitative Composition ◽

Combined Administration ◽

Osteoarthritis Progression ◽

Experimental Osteoarthritis ◽

Gut Microbiota Composition

Osteoarthritis is a most widespread chronic degenerative joint disease that causes pain, cartilage deformation, and joint inflammation. Adverse alterations of intestinal microbiota like dysbiosis may lead to metabolic syndrome and inflammation, two important components of osteoarthritis progression. Aim. In this study we investigated the effect of chondroitin sulfate and probiotics on the gut microbiome in monoiodoacetate-induced osteoarthritis model in rats. Methods. The species and quantitative composition of feces were determined using diagnostic media with selective properties. Further identification of isolated microorganisms was carried out according to morphological, tinctorial, physiological and metabolic parameters. The results are presented in the form of lg CFU/g. Results. Induction of osteoarthritis caused significant increasing the number of opportunistic enterobacteria and lactose-negative Escherichia coli against the decreasing of lacto- and bifidobacteria that may indicate a dysbiotic condition. Coadministration of chondroitin sulfate and probiotic bacteria has led to improvement the quantitative composition of the gut microbiota in experimental animals, the numerous of Bifidobacterium, Lactobacillus were increasing against decreasing the quantitative composition of opportunistic microorganisms. Conclusions. Monoiodoacetate-induced osteoarthritis caused dysbiosis of gut in rat. We observed beneficial effect of combined administration of chondroitin sulfate and probiotics on gut microbiota composition in rats with experimental osteoarthritis. Thus, adding of supplements like probiotics to standard treatment of osteoarthritis may have potentials to prevent and treat this disease.

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