Objective To observe the effect of acupuncture plus rehabilitation in treating deglutition disorders due to cerebral stroke and its effect on each link of the neural pathway of deglutition function. Method By adopting the prospective randomized controlled method, ninety-nine patients with deglutition disorders after cerebral stroke were recruited and divided into an acupuncture-rehabilitation group, a pharyngeal acupuncture group, and a control group, respectively 33 cases, 34 cases, and 32 cases in each group. The acupuncture-rehabilitation group was intervened by acupuncture respectively at scalp, pharyngeal, and the root of tongue plus basic treatment, the pharyngeal acupuncture group was by acupuncture at the deglutition point (Extra) plus basic treatment, while the control group was by the basic treatment alone, once a day, 4 weeks in total. The Functional Oral Intake Scale (FOIS) and Clinical Nursing Swallowing Assessment Tool (CNSAT) were evaluated and statistically analyzed before and after intervention. Result The component scores of CNSAT were significantly improved after intervention in the acupuncture-rehabilitation group (P<0.01); the component scores of CNSAT were significantly changed after intervention in the pharyngeal acupuncture group (P<0.05);the CNSAT component scores in the acupuncture-rehabilitation group were significantly different from that in the pharyngeal acupuncture group and control group after intervention (P<0.01); the CNSAT component scores in the pharyngeal acupuncture group were significantly different from that in the control group after intervention (P<0.05). The FOIS scores were enhanced in the three groups after treatment; the FOIS score was significantly changed in the acupuncture-rehabilitation group after intervention (P<0.01);the FOIS score was markedly changed in the pharyngeal acupuncture group after intervention (P<0.05);the FOIS scores in the acupuncture-rehabilitation group and pharyngeal acupuncture group were both significantly higher than that in the control group (P<0.01,P<0.05). Conclusion The scalp-pharyngeal-root of tongue sequential-acupuncture plus rehabilitation can effectively mitigate the deglutition problems after cerebral stroke, improve the food-intake ability of the patients, and reduce the risk of mistake inhalation.

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl₄). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl₄ solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl₄-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.
Animals ; Dogs ; Antioxidants/metabolism* ; Carbon Tetrachloride ; Chemical and Drug Induced Liver Injury/drug therapy* ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Liver ; Metabolic Networks and Pathways ; Mitochondria/metabolism* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Polysaccharides/pharmacology* ; Lycium/chemistry*