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Journal Article
Research Support, Non-U.S. Gov't
Ameliorating effects and mechanisms of chronic electroacupuncture at ST36 in a rodent model of dyspepsia induced by cisplatin.
Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society 2019 January
BACKGROUND: Chemotherapy-associated dyspepsia syndrome (CADS) is among the most intensive side effects and critical concerns for patients with cancer. To investigate the effects and mechanisms of chronic electroacupuncture (EA) at ST36 on chemotherapy-associated dyspeptic symptoms (CADS) in rats.
METHODS: Cisplatin (8 mg/kg, ip) was given once to establish CADS model. EA or sham-EA treatment was then performed one hour daily for 21 days.
KEY RESULTS: (a) EA treatment decreased kaolin intake within 24 hours (1.67 ± 0.23 g vs 2.36 ± 0.37 g in sham-EA, P < 0.05); EA increased food intake (9.43 ± 2.28 vs 4.32 ± 1.26 in sham-EA, P < 0.05) and cisplatin-induced reduction of body weight (426.38 ± 13.25 vs 407.92 ± 13.26 in sham-EA, P = 0.05). (b) The incidence of normal behavioral satiety sequence (53%) in EA group was greater than that in sham-EA (32%) group (X2 = 17.68, P < 0.01). (c) EA increased the percentage of normal gastric slow waves (82.6 ± 5.98 vs 22.8 ± 1.90 in sham-EA, P < 0.05). (d) EA normalized cisplatin delayed gastric emptying (71.3% ± 6.8% vs 44.6% ± 11.2% in control, P < 0.05). (e) EA decreased ratio of heart rate variability (0.30 ± 0.03 vs 0.56 ± 0.05 in sham-EA, P < 0.05). (f) EA decreased fasting ghrelin, glucagon-like peptide-1 and peptide YY (P < 0.01 vs sham-EA for all).
CONCLUSIONS AND INFERENCES: Chronic EA ameliorates dyspepsia symptom and improves gastric dysmotility induced by Cisplatin, mediated via the vagal and gastrointestinal hormonal mechanisms.
METHODS: Cisplatin (8 mg/kg, ip) was given once to establish CADS model. EA or sham-EA treatment was then performed one hour daily for 21 days.
KEY RESULTS: (a) EA treatment decreased kaolin intake within 24 hours (1.67 ± 0.23 g vs 2.36 ± 0.37 g in sham-EA, P < 0.05); EA increased food intake (9.43 ± 2.28 vs 4.32 ± 1.26 in sham-EA, P < 0.05) and cisplatin-induced reduction of body weight (426.38 ± 13.25 vs 407.92 ± 13.26 in sham-EA, P = 0.05). (b) The incidence of normal behavioral satiety sequence (53%) in EA group was greater than that in sham-EA (32%) group (X2 = 17.68, P < 0.01). (c) EA increased the percentage of normal gastric slow waves (82.6 ± 5.98 vs 22.8 ± 1.90 in sham-EA, P < 0.05). (d) EA normalized cisplatin delayed gastric emptying (71.3% ± 6.8% vs 44.6% ± 11.2% in control, P < 0.05). (e) EA decreased ratio of heart rate variability (0.30 ± 0.03 vs 0.56 ± 0.05 in sham-EA, P < 0.05). (f) EA decreased fasting ghrelin, glucagon-like peptide-1 and peptide YY (P < 0.01 vs sham-EA for all).
CONCLUSIONS AND INFERENCES: Chronic EA ameliorates dyspepsia symptom and improves gastric dysmotility induced by Cisplatin, mediated via the vagal and gastrointestinal hormonal mechanisms.
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