scholarly journals Effect of atractylenolide III on interstitial cells of Cajal and C-kit/SCF pathway of rats with loperamide-induced slow transit constipation

2021 ◽  
Vol 18 (6) ◽  
pp. 1197-1204
Author(s):  
Wang Hao ◽  
Gong Yuxia ◽  
Li Youran ◽  
Xu Minmin ◽  
Gu Yunfe
Keyword(s):  
Smooth Muscle ◽  
Western Blot ◽  
Smooth Muscle Cells ◽  
Slow Transit Constipation ◽  
Model Group ◽  
Rt Pcr ◽  
Mucous Layer ◽  
Slow Transit ◽  
Transit Constipation ◽  
Atractylenolide Iii

Purpose: To determine the effect of atractylenolide-III (ATL-III) on loperamide-induced slow transit constipation (STC) in a rat STC model, and to elucidate the mechanisms involved. Methods: Male Wistar rats were divided into five groups (n=6 per group): normal control group (NG), model group, and three STC rat groups treated with different doses of ATL-III, viz, 5, 10 and 15 mg/kg. The rats were treated for 15 days. Feed consumption, fecal excretion and intestinal transit rate were determined. Nitric oxide synthase (NOS), somatostatin (SS), serotonin (5-HT), and vasoactive intestinal peptide (VIP) were measured with enzyme-linked immunosorbent assay (ELISA). The protein and mRNA expressions of C-kit, SCF, PKC, and PI-3K were assayed using Western blot analysis and realtime reverse transcription polymerase chain reaction (RT-PCR), respectively. Results: The amount, weight, and moisture content of stool, and water consumption were significantly higher in ATL-III-treated groups than in the untreated (model) group (p < 0.05), whereas no difference was observed in feed intake. Intestinal transit rate was higher in the ATL-III-treated groups (p < 0.05). Decreased NOS, SS and VIP levels and increased 5-HT level were seen in the ATL-III-treated groups (p < 0.05). ATL-III treatment also induced increases in smooth muscle cells, neuronal cells, and mucous layer (p<0.05). Results from RT-PCR and Western blot revealed that ATL-III–treated groups had elevated c-kit, SCF, PKC, as well as PI-3K mRNA and protein expressions (p < 0.05). Conclusion: These results suggest that ATL-III mitigates loperamide-induced STC in rats via stimulation of NOS, SS, VIP, and 5-HT secretions. It also increases smooth muscle cells, neuronal cells, and mucous layer, and regulates the signaling pathways involving PKC, PI3K, SCF, and c-kit.

An Experimental Study on Intestine Transmission Function in SD Rats With Slow Transit Constipation After Electro-acupuncture Treatment in BL32 Acupoints

2021 ◽  
Author(s):  
Mu-Wen Qu ◽  
Ling-Ling Yuan ◽  
Fei Jia ◽  
Jun-Yi Li
Keyword(s):  
Acupuncture Treatment ◽  
Transmission Function ◽  
Dry Weight ◽  
Smooth Muscle Contraction ◽  
Slow Transit Constipation ◽  
Model Group ◽  
Contraction Amplitude ◽  
Sd Rats ◽  
Slow Transit ◽  
Transit Constipation

<B>Objective:</B>This study aims to use loperamide by gavage in SD rats to establish the model of STC, and evaluate the degree of similarity between the model and clinical diseases. Furthermore, the effect of electro-acupuncture when stimulating BL32 acupoints in SD rats with slow transit constipation were observed to determine changes in intestinal transmission function. <B>Methods:</B>Thirty SD rats were selected and divided randomly into three groups. Rats in the model group were given 2 mg/kg/d of loperamide tablets by gavage for 15 days. The morphology of the feces of rats was observed, and the dry weight of the feces and the time of first black feces movement with black ink by gavage after molding were measured. After 20 days of electro-acupuncture treatment at the BL32 acupoint, the time of first black feces movement, the ratio of black ink length of the entire length of the intestine, and contraction amplitude and frequency of contraction were measured. <B>Results:</B> The time of black feces movement in the two model groups was significantly prolonged (P<0.05).Furthermore, fecal grains, dry weight and moisture content were significantly reduced (P<0.05). On the 10thand 20thday of treatment, the time of black feces movementin the treatment group significantly decreased (P<0.05). The ratio of black ink length of the entire length of the intestine in the electro-acupuncture group was significantly higher than that in the model group (P<0.05). Moreover, contraction amplitude was significantly higher than in the model control group (P<0.05). <B>Conclusion:</B> Through loperamide gavage, the model of slow transit constipation in SD rats was successfully established in a relatively short period of time. Electro-acupuncture treatment had a rapid onset of action, and its mechanism might have been caused through strengthening the ability of intestinal smooth muscle contraction, and are independent with increased smooth muscle contraction frequency.

scholarly journals Colonic electrical stimulation promotes colonic motility through regeneration of myenteric plexus neurons in slow transit constipation beagles

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Yongbin Wang ◽  
Qian Wang ◽  
Kudelaidi Kuerban ◽  
Mengxue Dong ◽  
Feilong Qi ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Electrical Stimulation ◽  
Western Blot ◽  
Myenteric Plexus ◽  
Pulse Train ◽  
Colonic Motility ◽  
Slow Transit Constipation ◽  
Slow Transit ◽  
Transit Constipation ◽  
Colonic Electrical Stimulation

Abstract Slow transit constipation (STC) is a common disease characterized by markedly delayed colonic transit time as a result of colonic motility dysfunction. It is well established that STC is mostly caused by disorders of relevant nerves, especially the enteric nervous system (ENS). Colonic electrical stimulation (CES) has been regarded as a valuable alternative for the treatment of STC. However, little report focuses on the underlying nervous mechanism to normalize the delayed colonic emptying and relieve symptoms. In the present study, the therapeutic effect and the influence on ENS triggered by CES were investigated in STC beagles. The STC beagle model was established by oral administration of diphenoxylate/atropine and alosetron. Histopathology, electron microscopy, immunohistochemistry, Western blot analysis and immunofluorescence were used to evaluate the influence of pulse train CES on myenteric plexus neurons. After 5 weeks of treatment, CES could enhance the colonic electromyogram (EMG) signal to promote colonic motility, thereby improving the colonic content emptying of STC beagles. HE staining and transmission electron microscopy confirmed that CES could regenerate ganglia and synaptic vesicles in the myenteric plexus. Immunohistochemical staining showed that synaptophysin (SYP), protein gene product 9.5 (PGP9.5), cathepsin D (CAD) and S-100B in the colonic intramuscular layer were up-regulated by CES. Western blot analysis and immunofluorescence further proved that CES induced the protein expression of SYP and PGP9.5. Taken together, pulse train CES could induce the regeneration of myenteric plexus neurons, thereby promoting the colonic motility in STC beagles.

PPARγagonist Inhibited the Expression of β-Catenin in Rabbit Abdominal Aortic Artery Atherosclerotic Plaque with Hypercholesterolemia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3931-3931
Author(s):  
Miao Jiang ◽  
Yulin Wang ◽  
Xia Bai ◽  
Changgeng Ruan
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Immunohistochemical Analysis ◽  
Muscle Cells ◽  
Model Group ◽  
Rt Pcr ◽  
Balloon Injury ◽  
Abdominal Aortic ◽  
Aortic Artery

Abstract Objective: Atherosclerosis is a chronic inflammatory process; it involved T lymphoid cells and mono-macrophages adhesived and migrated to under endothelium, after phagocytosing LDL-cholesterol and become foam-cells. Moreover, T cells and macrophages secrets matrix metalloproteinase then promote smooth muscle cells migrating to beneath endothelium; and smooth muscle cells differentiated, proliferated and secreted extracellular matrix to form atherosclerotic plaque. All these factors resulted to vascular remodeling and atherosclerotic plaque formation. β-catenin is a important signal protein involved in controlling VSMC differentiation, proliferation, and fate, which can move to the nucleus, where it forms a complex with the TCF/LEF transcription factors to drive their target genes such as C-myc and cyclin D1, Cyclin D1 contains a Tcf response element within its promoter region and is thought to be a rate-limiting mediator of the G1 to S phase transition in the cell cycle. PPARagonist has been reported to inhibit mouse artery intima proliferation after balloon injury, moreover, PPARγagonists could have anti-atherosclerosis development in animal models, and also they could decrease the thickness of intima-media of carotid artery in patients with diabetes mellitus. In this research, we are aimed to investigate if PPARγagonist could inhibit the artery remodeling with hypercholesterolemia and vascular injury, in addition with the expression of β-catenin in remodeling artery. Methods: 12 New Zealand male rabbits weighting 2 to 2.5 kg were given hypercholesterol chows for 2 weeks, and then catheter balloon injury was performed in the rabbit abdominal aortic artery. all rabbits were randomized to model group and rosiglitazone group, hypercholesterol chows were continued to give to all rabbits for another 4 weeks, and rosiglitazone group was given rosiglitazone 3mg/kg/d for 4 weeks. Animals were euthanized by pentobarbital overdose at 28 days after balloon injury. Abdominal arteries were harvested. Immunohistochemical analysis, reverse transcription-polymerase chain reaction (RT-PCR) and western blot were used to detect the expression of β-catenin in rabbit abdominal aortic artery. Results: The thickness of intima-media in rosiglitazone group were significantly decreased than in hypercholesterolemia model group (1.048±0.076 vs 0.689±0.203mm p&lt;0.001), also there were much less foam cells in atherosclerotic plaque in rosiglitazone group compared with hypercholesterolemia model group. Immunohistochemical analysis showed that there were many smooth muscle cells migrated and proliferated in the neointimal of remodeling artery, and there was much less stain for β-catenin in rosiglitazone group than in hypercholesterolemia model group. And both RT-PCR and western blot showed that the expression of mRNA and protein of β-catenin were significantly decreased in rosiglitazone group compared with hypercholesterolemia model group. Conclusion: Hypercholesterolemia and vascular balloon injury are two important factors for smooth muscle cells migration and proliferation from medial; β-catenin expressed in the neointimall and might promote the formation of atherosclerosis; PPARγagonist not only inhibited the thickness of atherosclerotic plaque, but also significantly inhibited the expression of β-catenin; it might imply that the anti-atherosclerosis mechanism of PPARγ agonist may involve with β-catenin pathway.

Smooth muscle inclusion bodies in slow transit constipation

2001 ◽  
Vol 193 (3) ◽  
pp. 390-397 ◽  
Author(s):  
Charles H. Knowles ◽  
Carole D. Nickols ◽  
S. Mark Scott ◽  
Nick I. Bennett ◽  
Ricardo Brandt de Oliveira ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Inclusion Bodies ◽  
Slow Transit Constipation ◽  
Slow Transit ◽  
Transit Constipation

Progesterone receptor A mediates VIP inhibition of contraction

2010 ◽  
Vol 298 (3) ◽  
pp. G433-G439 ◽  
Author(s):  
Ling Cheng ◽  
Piero Biancani ◽  
Jose Behar
Keyword(s):  
Progesterone Receptor ◽  
Guinea Pig ◽  
Western Blot ◽  
G Proteins ◽  
Muscle Cells ◽  
Slow Transit Constipation ◽  
Protein Levels ◽  
Human Control ◽  
Slow Transit ◽  
Transit Constipation

The slow transit time of the colon in females with constipation is due to impairment of agonist-induced contraction. The impairment is associated with downregulation of G proteins that mediate contraction and upregulation of Gs proteins that mediate relaxation. These changes are caused by overexpression of progesterone (P4) receptors in the colon, rendering its muscle cells sensitive to physiological P4 concentrations. Downregulation of Gq/11 is mediated by P4 receptor B (PR-B). We examined whether upregulation of Gs proteins increased the inhibition of contraction and whether the increase is mediated by the P4 receptor A (PR-A). These studies were conducted in colon-isolated colon muscle cells from human control and slow-transit constipation (STC) females and from guinea pigs. Muscle cell contraction was induced by CCK-8. Inhibition of contraction was induced by vasoactive intestinal polypeptide (VIP), and 8′bromo-c′AMP (8B-c′AMP) G protein levels were determined by Western blot. VIP-induced inhibition of contraction was greater in muscle cells from STC and P4-treated muscle cells. There were no differences in the inhibition induced by 8B-c′AMP between muscle cells from STC and P4-treated controls. The increased VIP-induced inhibition of muscle cells treated with P4 was blocked by pretreatment with PR-A antibodies and unaffected by PR-B antibodies. These antibodies had no effect on 8B-c′AMP induced-inhibition. The P4 upregulation of Gs proteins was blocked by PR-A antibodies and unaffected by PR-B antibodies. Similar results were obtained in muscle cells from guinea pig colons. We concluded that P4 upregulation of Gs proteins increases VIP-induced inhibition of contraction mediated by PR-A.

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