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Hyperglycemia can cause early damage to human bady and develop into diabates that will severely threaten human healthy. The effectively clinical treatment of hyperglycemiais is by inhibiting the activity of α-amylase. Black tea has been reported to show inhibitory effect on α-amylase and can be used for hyperglycemia treatment. However, the mechanism underlying is unclear. In this study, in vivo experiment showed that black tea theaflavins extract (BTE) effectively alleviated hyperglycemia. In vitro experiment showed that the effects may be caused by the interation between theaflavins and α-amylase. While TF1 and TF3 were mixed type inhibitors of α-amylase, TF2A and TF2B were competitive inhibitors of α-amylase. Molecular docking analysis showed that theaflavins monomers interacted with the hydrophobic region of α-amylase. Further study verified that monomer-α-amylase complex was spontaneously formed depending on hydrophobic interactions. Taken together, theaflavins showed potential anti-hyperglycemia effect via inhibiting α-amylase activity. Our results suggested that theaflavins might be utilized as a new type of α-amylase inhibitor to prevent and cure hyperglycemia.

Learning and memory disorder is a cluster of symptoms caused by neuronal aging and other diseases of the central nervous system (CNS). Panax notoginseng saponins (PNS) are a series of saponins derived from the natural active ingredients of traditional Chinese medicine (TCM) that have neuroprotective effects on the central nervous system. In this paper, we review the ameliorative effects and mechanisms of Panax notoginseng saponin-like components on learning and memory disorders to provide valuable references and insights for the development of new drugs for the treatment of learning and memory disorders. Our summary results suggest that Panax ginseng saponins have significant effects on improving learning and memory disorders, and these effects and potential mechanisms are mediated by their anti-inflammatory, anti-apoptotic, antioxidant, β-amyloid lowering, mitochondrial homeostasis in vivo, neuronal structure and function improving, neurogenesis promoting, neurotransmitter release regulating, and probiotic homeostasis in vivo activities. These findings suggest the potential of Panax notoginseng saponin-like constituents as drug candidates for improving learning and memory disorders.

Physalis Calyx seu Fructus is the dry calyx or the calyx with fruit of the Solanaceae plant Physalis alkekengi L. var. franchetii (Mast.) Makino, with a long history of use in medicine and food. However, despite its many potential therapeutic and culinary applications, P. alkekengi is not being exploited for these applications on a large scale. This study analysed various research related to the different chemical components of P. alkekengi, including steroids, flavonoids, alkaloids, phenylpropanoids, sucrose esters, piperazines, volatile oils, polysaccharides, amino acids, and trace elements. In addition, research related to the pharmacological activities of P. alkekengi, including its anti-inflammatory, anti microbial, antioxidative, hypoglycaemic, analgesic, anti-tumour, and immunomodulatory effects were investigated. Research articles from 1974 to 2023 were obtained from websites such as Google Scholar, Baidu Scholar, and China National Knowledge Infrastructure, and journal databases such as Scopus and PubMed, with the keywords such as Physalis alkekengi, components, effects, and activities. This study aims to provide a comprehensive understanding of the progress of phytochemical and pharmacological research on the phytochemical and pharmacological aspects of P. alkekengi and a reference for the better exploitation of P. alkekengi in the food and pharmaceutical industries.

In this study, ultrasound-assisted extraction of flavonoid from Crinum asiaticum was studied through response surface methodology (RSM) to gain the best extraction process of flavonoid and enhance the extraction rate of flavonoid. In the following RSM experiment, we selected the corresponding data of every factor as the center point through the single-factor experiments, then the experimental data was subjected to multiple regression analysis. According to the statistical analysis results, the results were consistent with the polynomial regression model, the determination coefficient (R2) was 0.9769. The best conditions for maximum flavonoid yield were 60% ethanol concentration, 64 °C for extraction temperature, 1:28 (v/w) solid-to-liquid ratio with extraction time for 47 min. The best response of flavonoid yield was 1.63972%. The predicted results for best reaction conditions were in good agreement with experiment values. Ultrasound-assisted extraction method can enhance the extraction rate of flavonoid significantly. It is a powerful tool to extract of important phytochemicals from nature plant. Keywords: Ultrasound-assisted extraction, Flavonoid, Crinum asiaticum, Response surface methodology

Chronic hepatitis (CH) encompasses a prevalent array of liver conditions that significantly contribute to global morbidity and mortality. Yiguanjian (YGJ) is a classical traditional Chinese medicine with a long history of medicinal as a treatment for CH. Although it has been reported that YGJ can reduce liver inflammation, the intricate mechanism requires further elucidation. We used network pharmacology approaches in this work, such as gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and network-based analysis of protein-protein interactions (PPIs), to clarify the pharmacological constituents, potential therapeutic targets, and YGJ signaling pathways associated with CH. Employing the random walk restart (RWR) algorithm, we identified GNAS, GNB1, CYP2E1, SFTPC, F2, MAPK3, PLG, SRC, HDAC1, and STAT3 as pivotal targets within the PPI network of YGJ-CH. YGJ attenuated liver inflammation and inhibited GNAS/STAT3 signaling in vivo. In vitro, we overexpressed the GNAS gene further to verify the critical role of GNAS in YGJ treatment. Our findings highlight GNAS/STAT3 as a promising therapeutic target for CH, providing a basis and direction for future investigations.

Cl− movement and Cl−-sensitive signal pathways contributes to the survival and switch of inflammatory phenotype of microglia and are believed to play a key role in the inflammatory brain injury after ischemic stroke. Here, we demonstrated an important role of Cl− transmembrane transporter Swell1, in the survival and M2-like polarization of microglia in ischemic stroke. Knockdown or overexpression of Swell1 in cultured microglia inhibited or increased hypotonic-activated Cl− currents, respectively, and these changes were completely blocked by the volume-regulated anion channels (VRACs) inhibitor DCPIB. Swell1 conditional knock-in mice promoted microglia survival in ischemic brain region and resulted in significant reductions in neural cell death, infarction volume and neurological deficits following transient middle cerebral artery occlusion (tMCAO). Using gene manipulating technique and pharmacological inhibitors, we further revealed that Swell1 opening led to SGK1 (a Cl−-sensitive kinase)-mediated activation of FOXO3a/CREB as well as WNK1 (another Cl−-sensitive kinase)-mediated SPAK/OSR1-CCCs activation, which promoted microglia survival and M2-like polarization, thereby attenuating neuroinflammation and ischemic brain injury. Taken together, our results demonstrated that Swell1 is an essential component of microglia VRACs and its activation protects against ischemic brain injury through promoting microglia survival and M2-like polarization.

Blood brain barrier (BBB) damage that occurs within the thrombolytic time window is increasingly appreciated to negatively impact the safety and efficacy profiles of thrombolytic therapy for ischemic stroke. However, the spatiotemporal evolution of BBB damage in this early stroke stage and the underlying mechanisms remain unclear. Here, we investigated the topographical distribution of BBB damage and its association with tissue injury within the first 3 h after ischemia onset and the roles of matrix metalloproteinase (MMP)-2/9 in this process. Rats were subjected to 1, 2, or 3 h of middle cerebral artery occlusion (MCAO) followed by 10 min reperfusion with fluorescence-labeled dextran as BBB permeability marker. Acute tissue infarction was evidenced by staining defect with triphenyltetrazolium chloride (TTC). Cerebral blood flow (CBF) was measured by magnetic resonance imaging. MMP-2/9 were assessed by gel and in situ zymography. After 2-h MCAO, dextran leakage was seen in the ischemic ventromedial striatum and the preoptic area which showed ~70% CBF reduction, and expanded to other MCA regions including the cortex after 3-h MCAO. Interestingly, high (2000 kDa) and low (70 kDa) molecular weight dextrans displayed almost identical leakage patterns. Different from BBB damage, tissue infarction was first seen in the ischemic dorsal striatum and the parietal/insular cortex which experienced ~90% CBF reduction. Increased gelatinolytic activity colocalized with dextran leakage, and MMP-2 was found to be the major enzymatic source on gelatin zymograms. Pretreatment with MMP inhibitor GM6001 significantly reduced dextran leakage induced by 2-h and 3-h MCAO. Taken together, our findings reveal substantial differences in the topographic distribution of BBB damage and tissue infarction within the first 3 h after MCAO onset. Unlike ischemic neuronal damage, BBB damage appears to develop faster in brain regions with moderately severe ischemia, and MMP-2 contributes to this early ischemic BBB damage.