1.The Effect of Chronic Stress on muc2 Protein Expression in Colonic Mucosa of Rats
Qiaoyun TONG ; Hesheng LUO ; Zongyao ZHU
Journal of Chinese Physician 2001;0(05):-
Objective To investigate the effect of chronic stress on the mucin secretion and muc2 protein content in goblet cells of rat colonic mucosa. Methods 24 healthy Wistar rats were randomly divided into 2 groups. Control group moved freely, experimental group was forced to undergo 2-hour-long immobilization stress per day for 14 days. The number of goblet cells containing mucus was determined by AB/PAS histochemical staining. The expression of muc2 protein was detected by immuohistochemical staining. Results Chronic stress decreased the number of goblet cells containing mucus, and down-regulated the expression of muc2 protein in goblet cells in rat colonic mucosa. Conclusion Chronic stress damaged the colonic epithelial barrier and functions of colonic goblet cells.
2.Experimental animal studies on skin irritation with Shexiang Anhe hemorrhoid ointment and hemorrhoidal proximity models
Xinghao ZHU ; Qingjia REN ; Ga ZHUO ; Shanshan LI ; Zongyao WU ; Mingsan MIAO ; Dongmei QI
Acta Laboratorium Animalis Scientia Sinica 2024;32(9):1114-1121
Objective To investigate the acute toxicity,irritation,and other effects of Shexiang Anhe hemorrhoid ointment on hemorrhoid-phased model rats by examining the TLR4/p38 MAPK/NF-κB signaling pathway.Methods Sixteen New Zealand rabbits were randomly divided into an intact skin Shexiang Anhe hemorrhoid ointment group,intact skin control group,broken skin Shexiang Anhe hemorrhoid ointment group,and broken skin control group,with four rabbits in each group.In the experimental group,20 g of Shexiang Anhe hemorrhoid ointment(1 g/mL)was evenly applied to an area on the rabbits depleted of hair,and an equal volume of solvent(mixture of glycerol,lanolin,and water)was evenly applied to the area on the backs of the rabbits in the control group once a day for 14 days.Another 40 rats were taken and randomly divided into a normal group,model group,Maillard group,and hemorrhoid cream group,with 10 animals in each group.The cream was applied once a day for 14 days.The acute toxicity of the cream in the intact and broken skin of rabbits was observed by hematoxylin and eosin staining and other method after treatment.In situ photographs were taken of the perianal tissues of rats with hemorrhoids to observe the efficacy of Shexiang Anhe hemorrhoid ointment,and the length and width of the ulcers were measured with vernier calipers to calculate the area.Quantitative real time polymerase chain reaction was used to detect the expression of TLR4,p38 MAPK,and NF-κB mRNA in the perianal tissues of the rats.Results Compared with rabbits in the control groups with intact or broken skin,rabbits in the administered group showed no significant difference in body mass.The mean values for the irritation evaluation points for Shexiang Anhe hemorrhoid ointment on rabbits with broken skin for 1 h,24 h,48 h,and 72 h were 1.5,1,0.5,and 0.25,respectively,showing there was no obvious skin irritation.In the hemorrhoidal rats,Shexiang Anhe hemorrhoid ointment treatment significantly reduced hemorrhoid symptoms after 14 days administration;the ulcer area was significantly smaller(P<0.05)and TLR4,p38 MAPK,and NF-κB mRNA levels were significantly lower compared with the findings in the model group(P<0.05).Conclusions Shexiang Anhe hemorrhoid ointment is a safe topical treatment with minimal acute toxicity and irritation to the skin and achieved good efficacy in the treatment of hemorrhoidal rats.Its mechanism of action may be related to the inhibition of the TLR4/p38 MAPK/NF-κB signaling pathway.
3.Study on effects and mechanism of Tibetan medicine Shanhu qishiwei pill in lowering blood lipid of hyperlipidemia model rats
Hua CHUN ; Dandan WEI ; Xinghao ZHU ; Zongyao WU ; DAWAZHABA
China Pharmacy 2022;33(1):46-50
OBJECTIVE To study the effects of Tibetan medi cine Shanhu qishiwei pill in lowering blood lipid of hyperlipidemia(HLP)model rats ,and to explore its mechanism primarily. METHODS According to their body weigh ,60 SD rats were randomly divide into normal group ,model group ,simvastatin group (positive control ,20 mg/kg)and Shanhu qishiwei pill low-dose,medium-dose and high-dose groups (50,100,200 mg/kg),with 10 rats in each group. Normal group was given conventional diet ,and other groups were given high-lipid diet to induce HLP model ,for consecutive 4 weeks. Administration groups were given relevant medicine intragastrically at the same time of modeling ;normal group and model group were given equal volume of normal saline intragastrically ,once a day ,for consecutive 4 weeks. After last administration ,the serum levels of TC ,TG, LDL-C and HDL-C were determined ;pathological changes of liver tissue were observed ;the protein expressions of AMPK , p-AMPK,LKB1,and HMGCR in liver tissue were detected in each group. RESULTS Low-dose,medium-dose and high-dose of Shanhu qishiwei pill could significantly reduce the serum levels of TC ,TG and LDL-C and protein expression of HMGCR in liver tissue(P<0.05),while significantly increased serum level of HDL-C ,phosphorylation level of AMPK ,protein expression of LKB 1 in liver tissue in HLP model rats (P<0.05);the pathological changes of liver tissue in HLP model rats were improved to different extents. CONCLUSIONS Shanhu qishiwei pill can reduce the blood lipid level of HLP model rats ,and its mechanism may be related to inhibiting the transmission of LKB 1/AMPK signal pathway and regulating lipid metabolism.
4.Intervention effect and mechanism of breviscapine on hepatic fibrosis in rats
Dandan WEI ; Shanshan LI ; Minghao ZHANG ; Yurun WEI ; Hongling WANG ; Shuangshuang CHAI ; Jingjing YIN ; Min ZHANG ; Han ZHAO ; Zongyao WU ; Kuicheng ZHU ; Qingbo WANG
China Pharmacy 2024;35(6):671-677
OBJECTIVE To investigate the intervention effect and potential mechanism of breviscapine on hepatic fibrosis (HF) in rats based on the transforming growth factor-β(1 TGF-β1)/Smad2/extracellular signal-regulated protein kinase 1(ERK1) and Kelch-like epichlorohydrin-associated protein 1(Keap1)/nuclear factor-erythroid 2-related factor 2(Nrf2)/heme oxygenase-1(HO-1) pathways. METHODS Totally 60 rats were randomly divided into normal control group, model group, breviscapine low-dose, medium-dose and high-dose groups (5.4, 10.8, 21.6 mg/kg), and colchicine group (positive control, 0.45 mg/kg), with 10 rats in each group, half male and half female. Except for the normal control group, HF model of the other groups was induced by carbon tetrachloride. Subsequently, each drug group was given corresponding medicine by gavage once a day for 28 days. The liver appearance of rats in each group was observed and their liver coefficients were calculated. The levels of alanineaminotransferase (ALT) and aspartate aminotransferase (AST)in serum, those of ALT, AST, superoxide dismutase (SOD),malondialdehyde (MDA) and glutathione peroxidase (GSH- Px) in liver tissue were detected. The liver tissue inflammatory and fibrotic changes were observed. The protein and mRNA expressions of TGF-β1, Smad2, ERK1, Nrf2, Keap1 and HO-in liver tissue were detected. RESULTS Compared with the normal control group, the model group showed large areas of white nodular lesions in the liver, obvious inflammatory cell infiltration and collagen fiber deposition. The body weight, the levels of SOD and GSH-Px in liver tissue, the protein and mRNA expressions of Nrf2 and HO-1 were significantly lowered in the model group (P<0.05); the liver coefficient, the percentage of Masson staining positive area, ALT and AST levels of serum and liver tissue, MDA level of liver tissue, the protein and mRNA expressions of TGF-β1, Smad2, ERK1 and Keap1 were significantly increased (P<0.05). Compared with the model group, the liver lesions of rats in each drug group were improved, and the above quantitative indexes were generally reversed (P<0.05). CONCLUSIONS Breviscapine has a good intervention effect on HF rats, which may be related to inhibiting TGF-β1/Smad2/ERK1 pathway for anti-fibrosis and regulating Keap1/Nrf2/HO-1 pathway to inhibit oxidative stress.