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We studied the influence of the mechanical properties of pectin hydrogels on acute inflammation and tissue repair after subcutaneous implantation. We used hard and soft pectin hydrogels. The results of histology and the analysis of serum-level cytokines demonstrated that the intensity of acute inflammation increased with increasing hardness of the pectin hydrogels. We also showed that the pectin hydrogels did not inhibit tissue repair. The results of the morphometric and texture analysis of the pectin hydrogels showed that the in vivo biodegradation kinetics of hard hydrogels were greater than those of soft pectin hydrogels. We also observed that on the surface of the hard and soft pectin hydrogels, a network of collagen fibers was formed. The surface of the pectin hydrogel was shown to prevent the adhesion of infiltrating inflammatory cells. The results of the in vitro experiments demonstrated that pectin hydrogels inhibited the functional activity of macrophages and minimally activated the complement system. Therefore, we showed that soft pectin hydrogels have low proinflammatory potential and can be used in surgery as a barrier material as prevention of adhesions in the abdominal cavity. The hard pectin hydrogel can be used in tissue engineering. The hard pectin hydrogels can be used in the reconstruction of skin because are overpopulated with collagen fibers and contribute to the formation of new connective tissue, their elasticity is comparable to the skin and can be adjusted. They are biodegradable, and no additional manipulation is required to remove them.

The main complication that may arise after surgery is the formation of adhesions. The current trend in the prevention of postoperative adhesions is the application of anti-adhesive barrier materials for the separation of wound tissue during the critical period of mesothelial repair and healing. In this work, cryogels based on pectin and chitosan were obtained by the ionic cryotropic gelation method. It was found that the Heracleum L. pectin cryogels are more elastic (73 ± 6 kPa) than the apple pectin cryogels (29 ± 11 kPa). The addition of chitosan with different physical and chemical characteristics did not significantly affect the elasticity of pectin–chitosan cryogels. The greatest swelling ability was achieved during in vivo incubation of Heracleum L. pectin cryogels and Heracleum L. pectin with reacetylated chitosan cryogels (17.1 ± 1.6 and 14.2 ± 2.0 g/g, respectively). It was found that the complete biodegradation of apple pectin cryogels occurred within 24 h of incubation in the rat abdominal cavity. Heracleum L. pectin cryogels were encapsulated in a fibrous capsule and detected in the abdominal cavity after 168 h. Maximum anti-adhesion effect was observed through the use of apple pectin cryogels (0 ± 0.5 score). Significant anti-adhesive effect was also observed through the use of apple pectin–reacetylated chitosan cryogels (1 ± 0.5 score). Due to the high anti-adhesive activity, such cryogels can be recommended for the development of a new barrier material for use in surgery. The potential anti-adhesive mechanism of apple pectin cryogels which may be attributed to a combination of barrier function and bioactivity of cryogels components was discussed.

An injectable hydrogel was obtained from the high methyl-esterified plum Prunus domestica L. (PD) pectin and calcium ions (Ca2+). PD hydrogel showed a weak gel-like behavior and could be squeezed out of the syringe with an injection force of ca. 9 N. PD hydrogel was not suitable for the NIH/3T3 fibroblast cell adhesion in vitro. The live/dead fluorescence and MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide) assays indicated that the PD hydrogel had a low cytotoxicity in relation to both the adhered and gel surrounding fibroblasts. PD hydrogel was found to inhibit adhesion formation in the sidewall defect-cecum abrasion rat model. In the control group, the occurrence of adhesion of the cecum to the peritoneal wall was found in seven of the total seven rats operated. Only four of the seven animals that were treated with the PD hydrogel were noted to have any adhesions. These adhesions were of a minimum grade of 1, 2, and 3 and were represented by a thin film that could be easily broken. The protective effect of PD hydrogel was found to be comparable with that of hyaluronic acid hydrogel used as a positive control. PD hydrogel appeared to possess enhanced in vivo residence stability on the injury sites compared to hyaluronic acid hydrogel as measured by staining of healing tissue with periodic acid-Schiff reagent. The data obtained offered the prospect for the development of the pectin-based gels as new barrier materials for surgery.

The anti-inflammatory activity of the citrus pectins, CU701 and CU201, with low and high degrees of methylesterification (LM and HM), respectively, was studied after oral administration in mice using three models of inflammation: acetic acid-induced colitis, cytokine production by blood leukocytes in response to lipopolysaccharide (LPS) and endotoxin shock. Oral administration of either CU701 or CU201 24 h before the infusion of acetic acid into the colon was found to prevent the progression of colitis. However, CU701 was found to decrease the adhesion of peritoneal granulocytes and their production of reactive oxygen species in colitic mice, whereas CU201 had no effect on granulocyte activity. Only CU701 was found to decrease tumour necrosis factor-α (TNF-α) release and to increase production of the anti-inflammatory cytokine interleukin-10 (IL-10) 24 h after oral administration in mice. CU201 had no effect on cytokine production. CU701, but not CU201, was found to improve the survival rate in mice that were subjected to a lethal dose of LPS. The present study demonstrates that LM pectin would be a more efficient anti-inflammatory agent than HM pectin upon oral administration. LM pectin was found to inhibit both local and systemic inflammation, whereas HM pectin was shown to prevent intestinal inflammation.

It has been shown that pectin polysaccharides from different plants, depending on their structure, can either protect the intestinal walls of mammals against damage and inhibit the development of inflammation or, on the contrary, have proinflammatory effects. At the same time, galacturonan isolated from any pectin, being the main carbohydrate chain (backbone) of its macromolecule, shows a marked anti-inflammatory effect. A decrease in the quantity of neutrophiles in the intestinal wall after induced inflammation indicates that the anti-inflammatory effects of pectins can be based on their influence on the functional activity of leukocytes.

The pectic polysaccharide named rauvolfian RS was obtained from the dried callus of Rauvolfia serpentina L. by extraction with 0.7% aqueous ammonium oxalate. Crude rauvolfian RS was purified using membrane ultrafiltration to yield the purified rauvolfian RSP in addition to glucan as admixture from the callus, with molecular weights 300 and 100–300 kD, respectively. A peroral pretreatment of mice with the crude and purified samples of rauvolfian (RS and RSP) was found to decrease colonic macroscopic scores, the total area of damage, and tissue myelope roxidase activity in colons as compared with a colitis group. RS and RSP were shown to stimulate production of mucus by colons of the colitis mice. RSP appeared to be an active constituent of the parent RS. The glucan failed to possess anti-inflammatory activity.

Earlier, we detected antiinflammatory action of comaruman, pectin of the marsh cinquefoil Comarum palustre L. This effect can be explained by new data concerning inhibition of adhesion of human neutrophils to fibronectin by comaruman and its fragments. The galacturonan backbone fragment of molecular mass >10 kD appears to be the active region of the comaruman macromolecule. Comaruman CP (50–200 μg/ml) was found to decrease adhesion of neutrophils stimulated by phorbol 12-myristate 13-acetate (PMA, 1.625 μM) and by dithiothreitol (DTT, 0.5 mM). The fragments of comaruman CP-H (100 kD), CP-H1 (10–50 kD), and CP-H2 (100 kD) obtained by acidic hydrolysis and representing regions of linear polygalacturonan are shown to inhibit neutrophil adhesion more than the crude pectin. A fragment CP-E (

The inhibition of the adhesion of neutrophils to fibronectin by the fragments of the main galacturonan chain of the following pectins was demonstrated: comaruman from the marsh cinquefoil Comarum polustre, bergenan from the Siberian tea Bergenia crassifolia, lemnan from the duckweed Lemna minor, zosteran from the seagrass Zostera marina, and citrus pectin. The parent pectins, except for comaruman, did not affect the cell adhesion. Galacturonans prepared from the starting pectins by acidic hydrolysis were shown to reduce the neutrophil adhesion stimulated by phorbol 12-myristate 13-acetate (1.625 microM) and dithiothreitol (0.5 mM) at a concentration of 50-200 microg/ml. The presence of carbohydrate chains with molecular masses higher than 300, from 100 to 300, and from 50 to 100 kDa in the galacturonan fractions was proved by membrane ultrafiltration.

To study isolation and chemical characterization of pectin derived from the common cranberry Vaccinium oxycoccos L. (oxycoccusan OP) and the testing of its preventive effect on experimental colitis.Mice were administrated orally with OP two days prior to a rectal injection of 5% acetic acid and examined for colonic damage 24 h later. Colonic inflammation was characterized by macroscopical injury and enhanced levels of myeloperoxidase activity measured spectrophotometrically with o-phenylene diamine as the substrate. The mucus contents of the colon were determined by the Alcian blue dye binding method. Vascular permeability was estimated using 4% Evans blue passage after i.p. injection of 0.05 mol/L acetic acid.In the mice treated with OP, colonic macroscopic scores (1.1+/-0.4 vs 2.7, P0.01) and the total square area of damage (10+/-2 vs 21+/-7, P0.01) were significantly reduced when compared with the vehicle-treated colitis group. OP was shown to decrease the tissue myeloperoxidase activity in colons (42+/-11 vs 112+/-40, P0.01) and enhance the amount of mucus of colitis mice (0.9+/-0.1 vs 0.4+/-0.1, P0.01). The level of colonic malondialdehyde was noted to decrease in OP-pretreated mice (3.6+/-0.7 vs 5.1+/-0.8, P0.01). OP was found to decrease the inflammatory status of mice as was determined by reduction of vascular permeability (161+/-34 vs 241+/-21, P0.01). Adhesion of peritoneal neutrophils and macrophages was also shown to decrease after administration of OP (141+/-50 vs 235+/-37, P0.05).Thus, a preventive effect of pectin from the common cranberry, namely oxycoccusan OP, on acetic acid-induced colitis in mice was detected. A reduction of neutrophil infiltration and antioxidant action may be implicated in the protective effect of oxycoccusan.

The efficacy of comaruman CP, a pectin of marsh cinquefoil Comarum palustre L., was investigated using a model of acetic acid-induced colitis in mice. Mice were administered comaruman CP orally 2 days prior to rectal injection of 5% acetic acid and examined for colonic damage 24 hr later. Colonic inflammation was characterized by macroscopical injury, higher levels of myeloperoxidase activity, enhanced vascular permeability, and diminution of colonic mucus. Oral administration of comaruman CP was found to prevent progression of colitis. Colonic macroscopic scores and the total square of damage were significantly reduced in mice treated with CP compared with the vehicle-treated colitis group. Peroral pretreatment of mice with comaruman CP was shown to decrease tissue myeloperoxidase activity in colons compared with the colitis group. Comaruman CP was found to stimulate production of mucus by colons of normal and colitis mice. Comaruman CP decreased the inflammatory status of normal mice as elicited by reduction of vascular permeability and adhesion of peritoneal neutrophils and macrophages. Thus, a preventive effect of comaruman on acetic acid-induced colitis in mice was detected. Reduction of neutrophil infiltration and enhancement of colon-bound mucus may be implicated in the protective effect of comaruman.