| Objective Studies were conducted to explore the modulatory role of lotus-seed milk fermentedproduct on gastrointestinal motility and absorbing and the protective effect of hepatic acutedamage in mouse, and to gather the information for utilizing the new efficacy of lotus-milkfermented product as dietary supplements.Method1. Mouse had been fed with distilled water, 25%, 50%, 75% lotus-seed milkfermented product and Domperidone for 10 days, intraperitoneal injected L-argininein the last 5 days. To observe the state of gastric emptying, small intestinal propellingafter gastric feed phenol red paste, mensurate the NO concentration of gastrichomogenate.2. Mouse had been fed with distilled water, 25%, 50% and 75%lotus-seed milkfermented product for 5 days. Gastric fed Compound Diphenoxylate to make themodel of constipation, measured time, weight and quantity and the water content ofblack feces excreted during 6 hours.3. Mouse had been hypodermic injected reserpine for 14 days, fed with distilledwater, 50%, 100%lotus-seed milk fermented product and JianWeiXiaoShiPian in thelast 7days. Observed the small intestinal propellant function and the content of xylosein urine collected in 5 hours.4. Ascertain the effect of lotus-seed milk fermented product on the peroxideproduction LPO of normal liver homogenate and normal hepatic homogenateexcitated by cysteine and ferrous sulfate in vitro. Mouse were fed with distilled water,25%, 50%, 100% lotus-seed milk fermented product and Vitaimn E, intraperitonealinjected carbon tetrachloride vegetal oil admixture in the 14th day. The examinesassessing the degree of the hepatic acute damage and peroxidization were executed.Pathomorphological changes were detected by haematoxylin eosin coloration andimmunohistochemistry.Result1. Percent of phenol red leaving in stomach and NO concentration of model groupwas increased compared with that in control group (p=0.024, p<0.001). Gastricemptying positive correlate with NO concentration , r=0.475, p=0.001. Percent ofphenol red leaving in stomach of 25%, 50%LMFP groups and Domperidone groupwere significantly decreased than those in model group (p=0.002, p=0.044, p=0.002);Percent of phenol red leaving in the forane small intestinal segments in model groupwas lower than that of control group (p=0.004,p=0.015,p=0.034), those in 50% LMFPgroup and Domperidone group were significantly increased (the last 3 small intestinalsegments: p=0.005, p=0.006;the last 4 small intestinal segments: p=0.034,p=0.001);Percent of phenol red leaving in the last 4 small intestinal segments in 75% LMFPgroup was significantly increased compared with that in model group (p=0.023).Theexamines clue on the accelerating of gastrointestinal propellant and modulatory effecton NO level.2. As compared with control group, weight and water content of black feces of modelgroup was significantly reduced (p=0.002, p<0.001), time of black feces excreted wassignificantly extended (p=0.001); Time of black feces excreted of 25%, 50%,75%LMFP groups was significantly reduced than that in model group(p=0.002,p=0.000,p=0.010); Weights of black feces excreted of 25% and 50% LMFPgroups were significantly increased than that in model group (p=0.008,p=0.005),water content of black feces of the all dosage LMFP groups was significantlyincreased than that in model group , all Significance<0.001.Results indicate theease-constipation of the LMFP.3. Xylose concentration in urine of reserpine group was decreased compared with thecontrol group (p=0.002); However, Xylose levels in 50%, 100% LMFP was higherthan those in model group by 30.10%, 55.73% (p=0.014, p<0.001). Percent of smallintestinal length of powdered charcoal paste propellanted in model group was higherthan that of negative group (p=0.033), that in 100%LMFP group was lower comparedwith the model group (p=0.002). It shows that high dosage LMFP slower accelerationof small intestinal propelling and promote absorbing in small intestine.4. LPO level of normal liver homogenate in 75%LMFP group was reduced comparedwith control group (p=0.003), LPO levels of normal hepatic homogenate excitated bycysteine and ferrous sulfate in 50% and 75% LMFP groups were significantlydecreased compared with the control group (p<0.001, p=0.003). LDH activity of CCl4group was higher than that of control group (p=0.010); ALT activity of 100%LMFPgroup and VE group was reduced by 8.17%, 14.17% (p=0.004, p<0.001); LDHactivity of all dosage LMFP and VE groups was significantly decreased comparedwith control group (p=0.007, p=0.008, p<0.001, p=0.007). Hepatocyte necrosis, fattydegeneration and inflammatory cells penetration of the LMFP and VE groups wererelieved compared with the model group. Compared with the model group, LPO levelof all LMFP and VE groups were significantly decreased by 50.15%, 53.78%,58.87%, 72.68% (all Significance<0.001) ; SOD activity of all LMFP and VE groupswas significantly increased by 48.68%, 59.16%, 65.76%, 49.30%( p=0.002, p<0.001,p<0.001, p=0.001).Bcl-2 express of all LMFP and VE groups enhanced comparedwith model group. LMFP can enhance anti-oxide ability, restrain the production ofperoxidization, relieve the degree of acute CCl4 hepatic damage.Conclusion1. The model of gastrointestinal dysfunction was established by intraperitonealinjecting L-arginine, gastric emptying positive correlate with NO concentration.2. LMFP can restrain the increase of gastric tissue NO concentration due to injectingL-arg by the dosage of 25% and 50%, accelerate gastric emptying, small intestinalpropelling. Studies were carried out to validate the ease-constipation of the LMFP.3. LMFP can slower the acceleration of small intestinal propelling due to injectingreserpine by the dosage of 100%, promote absorbing in small intestine.4. LMFP can protect liver from acute CCl4 hepatic damage by the mechanism ofanti-oxide system. |
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