OBJECTIVETo evaluate the effects of Tanguticum Maxim polysaccharide (TMP-1) on TNBS-induced colitis in rats.

METHODRats with TNBS/ethanol-induced colitis were used and treated with TMP-1 and dexamethasone (DX). Seventy-two rats, including animals with TNBS-induced colitis, were treated with saline, TMP-1 (100, 200, 400 mg.kg-1) and DX. White blood cells were counted on the fifth day and the rats were killed by ether on the sixth day. SOD activity in serum, MPO and SOD activity of colonic tissue were measured.

RESULTThe remarkable effects of TMP-1 at dosage of 200, 400 mg.kg-1 on TNBS-induced colitis were observed. The ulcerative area was diminished and weight of colon was reduced. White blood cell population was reduced, SOD activity in serum and SOD activity of colon tissue were remarkably increased, and, MPO activity of colonic tissue was reduced.

CONCLUSIONTMP-1 has significant effects on TNBS-induced colitis in rats with lower side effects, which suggests the effective component of rhubarb on colitis perhaps is TMP. The mechanism of the actions of TMP may relate to its antiflammation, antioxidation and immunoloregulation.

Animals ; Anti-Inflammatory Agents, Non-Steroidal ; therapeutic use ; Colitis, Ulcerative ; chemically induced ; drug therapy ; Colon ; enzymology ; pathology ; Male ; Phytotherapy ; Plants, Medicinal ; chemistry ; Polysaccharides ; isolation & purification ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Rheum ; chemistry ; Trinitrobenzenesulfonic Acid

The effect of electroacupuncture (EA) on experimental colitis was investigated in Sprague-Dawley rats. Colitis was induced by intracolonic instillation of 4% acetic acid. EA (2 Hz, 0.05 ms, 2 V for 20min) was applied to bilateral Hoku (LI-4) and Zusanli (ST-36) on 12 hrs and 36 hrs after induction of colitis. EA-treatment significantly reduced the macroscopic damage and the myeloperoxidase activity of colonic samples at 3 days post-induction of colitis. Colitic colon showed a decreased in vitro motility. However, colonic motility of EAtreated group was not significantly different from that of normal group. The anti-inflammatory effect of EA was not inhibited by a glucocorticoid receptor antagonist, RU-486, but suppressed by a beta-adrenoceptor antagonist, propranonol. These results suggest that EA-treatment has a beneficial effect on colitis, and its anti-inflammatory effect is mediated by beta-adrenoceptor activation but not by endogenous glucocorticoiddependent mechanism.
Acetic Acid ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Carbachol/pharmacology ; Cholinergic Agonists/pharmacology ; Colitis/chemically induced/enzymology/pathology/*therapy ; Electroacupuncture/*veterinary ; Enzyme Inhibitors/metabolism ; Gastrointestinal Motility/physiology ; Hormone Antagonists/pharmacology ; Male ; Mifepristone/pharmacology ; Muscle Contraction/physiology ; Muscle, Smooth/drug effects/physiology ; NG-Nitroarginine Methyl Ester/pharmacology ; Peroxidase/metabolism ; Propranolol/pharmacology ; Rats ; Rats, Sprague-Dawley