Pterostilbene could alleviate diabetic cognitive impairment by suppressing TLR4/NF-кB pathway through microbiota-gut-brain axis.

Diabetic cognitive impairment (DCI) is a serious neurodegenerative disorder caused by diabetes, with chronic inflammation being a crucial factor in its pathogenesis. Pterostilbene is a well-known natural stilbene derivative that has excellent anti-inflammatory activity, suggesting its potential medicinal advantages for treating DCI. Therefore, this study is to explore the beneficial effects of pterostilbene for improving cognitive dysfunction in DCI mice. A diabetic model was induced by a high-fat diet plus streptozotocin (40 mg·kg-1 ) for consecutive 5 days. After the animals were confirmed to be in a diabetic state, they were treated with pterostilbene (20 or 60 mg·kg-1 , i.g.) for 10 weeks. Pharmacological evaluation showed pterostilbene could ameliorate cognitive dysfunction, regulate glycolipid metabolism disorders, improve neuronal damage, and reduce the accumulation of ß-amyloid in DCI mice. Pterostilbene alleviated neuroinflammation by suppressing oxidative stress and carbonyl stress damage, astrocyte and microglia activation, and dopaminergic neuronal loss. Further investigations showed that pterostilbene reduced the level of lipopolysaccharide, modulated colon and brain TLR4/NF-κB signaling pathways, and decreased the release of inflammatory factors, which in turn inhibited intestinal inflammation and neuroinflammation. Furthermore, pterostilbene could also improve the homeostasis of intestinal microbiota, increase the levels of short-chain fatty acids and their receptors, and suppress the loss of intestinal tight junction proteins. In addition, the results of plasma non-targeted metabolomics revealed that pterostilbene could modulate differential metabolites and metabolic pathways associated with inflammation, thereby suppressing systemic inflammation in DCI mice. Collectively, our study found for the first time that pterostilbene could alleviate diabetic cognitive dysfunction by inhibiting the TLR4/NF-κB pathway through the microbiota-gut-brain axis, which may be one of the potential mechanisms for its neuroprotective effects.

Trilobatin alleviates non-alcoholic fatty liver disease in high-fat diet plus streptozotocin-induced diabetic mice by suppressing NLRP3 inflammasome activation.

Diabetes mellitus (DM) is a factor with great risk in the course of non-alcoholic fatty liver disease (NAFLD) due to its high glucotoxicity and lipotoxicity. Trilobatin, a glycosylated dihydrochalcone derived from the leaves of the Chinese sweet tea Lithocarpus polystachyus Rehd, is reported to possess various pharmacological activities. Nevertheless, it is still unclear regarding if trilobatin can alleviate liver injury in diabetic mice with NAFLD and its mechanism. Our aim was to investigative the protective effects of trilobatin against DM with NAFLD and its mechanism of action. A DM mice model was established by high-fat diet (HFD) feeding with streptozocin (STZ) injections, and treated with trilobatin for 10 weeks. The biochemical results showed that trilobatin restored glucose metabolic disorder and liver function in diabetic mice. The histopathological evaluation revealed that trilobatin improved liver injury by alleviating lipid accumulation and liver fibrosis. Mechanistically, trilobatin decreased expression of NLRP3, p65 NF-κB, cleaved-Caspase-1 and N-GSDMD, as well as the release of IL-18 and IL-1ß, leading to a alleviation of inflammation and pyroptosis. Taken together, we determined for the first time found that trilobatin could prevent liver injury in diabetic mice with NAFLD by suppressing NLRP3 inflammasome activation to reduce inflammation and pyroptosis.

A blink restoration system with contralateral EMG triggered stimulation and real-time artifact blanking.

Patients suffering from facial paralysis are on the hazard of disfigurement and loss of vision due to loss of blink function. Functional-electrical stimulation (FES) is one possible way of restoring blink and other functions in these patients. A blink restoration system for uni-lateral facial paralyzed patients is described in this paper. The system achieves restoration of synchronized blink through processing the myoelectric signal of orbicularis oculi at the normal side in real-time as the trigger to stimulate the paralyzed eyelid. Design issues are discussed, including EMG processing, stimulating strategies and real-time artifact blanking. Two artifact removal approaches based on sample and hold and digital filtering technique are proposed and implemented. Finally, the whole system has been verified on rabbit models.

Myoelectric signals of levator palpebrae superioris as a trigger for FES to restore the paralyzed eyelid.

Some closed loop FES systems have been designed to restore the blinking function of facial paralysis patients. All of them used myoelectric signal of orbicularis oculi at the normal side as the trigger to stimulate the paralyzed side. They were limited to the one side facial paralysis. Here we proposed that the myoelectric signal of levator palpebrae superioris could be used as the trigger to stimulate the paralyzed orbicularis oculi. Because the levator palpebrae superioris and the innervating nerve are intact, the myoelectric signal of the paralyzed side still could be used as the trigger. It will be more acceptable for the patients and have the potential to resolve the bilateral facial paralysis.

[Research progress in reanimation of peripheral facial paralysis by use of functional electrical stimulation].

With the development of electronics and information technology, the application of functional electrical stimulation in the medical field has been expanding. However, the use of functional electrical stimulation to treat patients with peripheral facial paralysis is still in its infancy. The main problems include: (1) Finding in the signals which could fire the stimulator; (2) Exploring the parameters for the stimulator; (3) The effects on the muscle attributed to the electrical stimulation. A review on these problems is presented.