Hemiplegia due to hypoglycaemia followed by haemicorea after correction of glycaemic values.

A 69-year-old man suffered from hemiplegia of the left limb due to hypoglycaemia. After 3 h of oral supplementation with sugar water, the patient recovered from hemiplegia but then presented symptoms of haemichorea. To our knowledge, a case of abnormal glucose metabolism complicated with two types of motor disturbance has not been reported previously.

LncRNA Meg3 promotes oxygen and glucose deprivation injury by decreasing angiogenesis in hBMECs by targeting the miR­122­5p/NDRG3 axis.

Oxygen-glucose deprivation (OGD) is widely used as an in vitro model for stroke. The present study aimed to explore the mechanisms of action of long non-coding RNA (lncRNA) maternally expressed gene 3 (Meg3) in angiogenesis following OGD. The human brain microvascular endothelial cell line, hCMEC/D3, was used to establish the OGD model. lncRNA Meg3 was highly expressed in hCMEC/D3 cells subjected to OGD. Furthermore, it was found that the overexpression of lncRNA Meg3 decreased the proliferation, migration and angiogenesis of hCMEC/D3 cells subjected to OGD, and increased cell apoptosis. Meg3 silencing exerted the opposite effects. Subsequently, lncRNA Meg3 increased the expression of NDRG family member 3 (NDRG3) by directly binding to miR-122-5p. The overexpression of miR-122-5p and the knockdown of NDRG3 reversed the inhibitory effects of Meg3 overexpression on the proliferation, migration and angiogenesis of hCMEC/D3 cells subjected to OGD, as well as the promoting effects of Meg3 overexpression on cell apoptosis. The present study demonstrated that lncRNA Meg3 functions as a competing endogenous RNA by targeting the miR-122-5p/NDRG3 axis in regulating OGD injury.

Effect and Mechanism of Yisui Fuyongtang (YSFYT) Decoction on Cognitive Function and Synaptic Plasticity in Rats with Vascular Cognitive Impairment.

Vascular cognitive impairment (VCI) has emerged as the second major disease responsible for dementia, and there is still a lack of effective treatment methods for this disorder to date. Clinical medications have found that Yisui Fuyongtang (YSFYT) Decoction is effective in improving neurological signs and learning-memory functions in patients who develop white matter lesions and whole brain atrophy. To clarify the effect and molecular regulation mechanism of YSFYT Decoction on model rats, this research analyzed the influence of YSFYT Decoction on the learning-memory ability and lipid metabolism of rats based on behavioral and biochemical analysis. Further pathology and protein detection methods were adopted to investigate the action of YSFYT Decoction on the neurons in the hippocampus of model rats and the regulation of the brain derived neurotrophic factor (BDNF)-tyrosine protein kinase receptor B (TrkB) signaling pathway. Compared with the VCI group, after YSFYT Decoction administration, the ratio of swimming time in the platform, number of crossing the platform, number of active avoidance, and proportion of active avoidance of the rats were markedly increased, whereas the response latency was substantially reduced (p < 0.05). Biochemical tests indicated that contents of lipoprotein lipase (LPL), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) of the model rats in YSFYT Decoction treatment group were greatly reduced, whereas those of total antioxidant capacity (T-AOC), glutathione peroxidase (GSH-PX), catalase (CAT), malondialdehyde (MDA), and superoxide dismutase (SOD) were elevated (p < 0.05). Additionally, Bcl-2 expression in YSFYT Decoction treatment group was significantly increased, but neuron apoptosis of the hippocampus tissue was reduced. Meanwhile, neuron number was apparently higher than that in VCI model group. Following Yisui Decoction treatment, expressions of growth-associated protein 43 (GAP43), synaptophysin (SYP), postsynaptic density 95 (PSD95), NMDAR subunit 2B (NR2B), BDNF, TrkB, phospho-mitogen-activated protein kinase (p-MAPK), extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K), and phospho-protein kinase B (p-AKT) were markedly elevated. Taken together, YSFYT Decoction could activate the BDNF-TrkB signaling pathway, elevate Bcl-2 expression, and minimize neuronal apoptosis in hippocampus, thereby improving the behavioral characteristics and biochemical indicators of the VCI rat model.

Effect of Yisui Multipurpose Soup's Amelioration on D-Galactose-Induced Neuronal Cells.

This study clarified the regulatory effect of Yisui multipurpose Soup towards D-galactose-induced cognitive impairment cell model on the molecular level. We first constructed and cultured the cell model of cognitive impairment induced by D-galactose in neurons in vitro and then cultured the cells in the medium supplemented with different doses of drug-containing serum of Yisui multipurpose soup. Expressions of inflammatory cytokine tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), nitric oxide (NO), and interleukin-1ß (IL-1ß) were assessed by the ELISA and western blot, and cell apoptosis was determined by flow cytometry and TUNEL. The expression changes of apoptosis-related proteins Bcl-2 and Bax were estimated by immunofluorescence, qPCR, and western blot. Finally, we analyzed and made the network interaction diagram of Yisui multipurpose soup-components-targets through the network pharmacology method, from which we could learn that there were 1104 gene targets related to vascular cognitive impairment (VCI) and 1071 component targets of Yisui multipurpose soup. And there were 251 overlapping genes, mainly gathering in protein binding, protein modification, MAPK signaling pathway, and calcium signaling pathway. The expressions of TNF-α, iNOS, NO, and IL-1ß were significantly decreased after the culture medium was replaced by medium containing drug serum. We also found that the effect of high-dose drug-containing serum on the expression of inflammatory factors was better than that of low dose. The Yisui multipurpose soup drug serum in the medium not only significantly increased Bcl-2 expression and effectively reduced Bax expression, but also inhibited the apoptosis of neurons induced by D-galactose. In conclusion, Yisui multipurpose soup could effectively protect D-galactose-induced neuronal cell cognitive impairment by orchestrating expressions of the inflammatory factors TNF-α, iNOS, NO, and IL-1ß and the apoptosis-related proteins Bcl-2 and Bax.

[Protective effect and immune mechanism of berberine on cerebral ischemia/reperfusion injury in rats].

Objective: To investigate the protective effect and immune mechanism of berberine on cerebral ischemia/reperfusion injury in rats. Methods: Fifty SD rats were randomly divided into sham operation group (Sham), model group (Model), berberine low dose groups (BBR-L, 25 mg/kg), berberine medium dose groups (BBR-M, 50 mg/kg) and berberine high dose groups (BBR-H, 100 mg/kg), with 10 rats in each group. Longa suture method was used to establish a rat model of cerebral ischemia/reperfusion, after 2 hours of ischemia, reperfusion for 24 hours. Rats in BBR-L, BBR-M and BBR-H were treated with berbrerine by gavage 2 hours after successful model building, while the sham operation group and the modle group were given the same volume of saline as described above. After 24 hours of administration, the activity of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), cytokine tumor necrosis factor α (TNF-α) , interferon ß (IFN-ß) , interleukin 6 (IL-6) and nitric oxide (NO) content were detected by ELISA assay. Serum CD4+, CD8+ and CD4+/CD8+ contents were measured by flow cytometry to investigate the immune function of each group. RT-qPCR and Western blot were used to detect NF-kappaB-NOD-like receptors 3 (NF-κB-NLRP3) signal axis key genes and protein expression in rat brain tissue. Results: Compared with the sham operation group, the degree of neurological deficit and the rate of cerebral infarction were increased in the model group (P＜0.05), and the levels of serum NO, TNF-α, IFN-ß, IL-6, NF-κB p65, NLRP3, ASC and caspase-1 in brain tissue were increased (P＜0.05), while the activities of SOD, GSH-Px and the levels of CD4+, CD8+ and CD4+/CD8+ in serum were decreased (P＜0.05). Compared with the model group, the degree of neurological deficit and the rate of cerebral infarction were increased in the BBR-H, BBR-M and BBR-L groups (P＜0.05), and the levels of serum NO, TNF-α, IFN-ß, IL-6, NF-κB p65, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1 in brain tissue were increased (P＜0.05), while the activities of SOD, GSH-Px and the levels of CD4+, CD8+ and CD4+/CD8+ in serum were decreased (P＜0.05). Conclusion: Berberine may reduce oxidative stress, inhibit inflammation, enhance immune function, and reduce cerebral ischemia/reperfusion injury in rats, which may be related to the inhibition of NF-κB-NLRP3 signaling.