The roots of Polygala tenuifolia Willd have a long history of being used as a traditional Chinese medicine for the treatment of insomnia, forgetfulness, sorrow and depression. This research show the special function in Alzheimer's disease.

Minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains unclear. In this study, we further investigated the effect and mechanism of S100B, predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model. We discovered that S100B expressions and autocrine were significantly increased in MHE rats and astrocytes isolated from MHE rats. Furthermore, we found that S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NFƙB, eventually resulting in inflammation and oxidative stress caused by MHE astrocytes. Compared to WT astrocytes, impairment of MHE astrocytes supported neuronal growth in co-culture. To sum up, comprehensive-understanding of the impact of S100B-overexpressed MHE astrocyte on MHE pathology may provide insights into the etiology of MHE.

Background: Our previous study revealed that minimal hepatic encephalopathy (MHE) is strongly associated with neuroinflammation. Nevertheless, the underlying mechanism of the induction of inflammatory response in MHE astrocytes remains unclear. Methods: In this study, we further investigated the effect and mechanism of S100B, predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model. Results: We discovered that S100B expressions and autocrine were significantly increased in MHE rats and astrocytes isolated from MHE rats. Furthermore, we found that S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NFƙB, eventually resulting in inflammation and oxidative stress caused by MHE astrocytes. Compared to WT astrocytes, impairment of MHE astrocytes supported neuronal growth in co-culture.Conclusions: To sum up, comprehensive-understanding of the impact of S100B-overexpressed MHE astrocyte on MHE pathology may provide insights into the etiology of MHE.

Background: Our previous study revealed that minimal hepatic encephalopathy (MHE) is strongly associated with neuroin ammation. Nevertheless, the underlying mechanism of the induction of in ammatory response in MHE astrocytes remains unclear.Methods: In this study, we further investigated the effect and mechanism of S100B, predominant isoform expressed and released from mature astrocytes, on MHE-like neuropathology in the MHE rat model.Results: We discovered that S100B expressions and autocrine were signi cantly increased in MHE rats and astrocytes isolated from MHE rats. Furthermore, we found that S100B stimulates VEGF expression via the interaction between TLR2 and RAGE in an autocrine manner. S100B-facilitated VEGF autocrine expression further led to a VEGFR2 and COX-2 interaction, which in turn induced the activation of NF B, eventually resulting in in ammation and oxidative stress caused by MHE astrocytes. Compared to WT astrocytes, impairment of MHE astrocytes supported neuronal growth in co-culture. Conclusions: To sum up, comprehensive-understanding of the impact of S100B-overexpressed MHE astrocyte on MHE pathology may provide insights into the etiology of MHE. Background Minimal hepatic encephalopathy (MHE) is characterized by a speci c, complex mild cognitive impairment. Attention de cits, psychomotor slowing, and impaired bimanual and visuomotor coordination are among the few key features [1, 2]. A previous study has suggested that pro-in ammatory cytokines released from astrocytes participate in the regulation of pathogenesis of MHE [3]. However, the underlying mechanism of the induction of in ammatory response in MHE astrocytes remains unclear. S100 calcium-binding protein B (S100B) is a predominant isoform of the S-100 protein family [4], mainly expressed and released from mature astrocytes [5][6]. Secreted S100B exerts an autocrine effect on astrocytes [7], being toxic at high concentrations [8]. Astrocytic S100B acts as a perpetrator of the noxious cytokine cycle, associated with maladaptive astrocytic activation [12][13]. Micromolar S100B levels, which can turn astrocytes into a pro-in ammatory neurodegenerative phenotype, are an important source of in ammatory cytokines [10] that induce TNFα secretion [9]. Overexpression and knockout of S100B have been associated with exacerbation and attenuation of brain damage, respectively [14]. The activated astrocytes' responses to neuronal damage or dysfunction re ected in AD brain markedly overexpress intercellular biologically active S100B [15][16]. However, so far, no studies have reported on the production of S100B by astrocytes in MHE rats and the underlying mechanism by the autocrine action of S100B on pro-in ammatory response.

Background: The mechanism underlying the impaired cognitive function and memory loss in Minimal hepatic encephalopathy (MHE) remains unclear. Dopamine (DA) is reported to be associated with dementia. Methods: In this study, we investigated mechanism underlying DA-induced MHE pathology by immunoblotting, ELISA, FM4-64 and fluorescence staining. Results: We observed that MHE brains showed the increased content of DA, after administration of anti-DA antibody, and cognitive loss in MHE rats was recovered to the normal level, indicating the involvement of DA in the pathogenesis of MHE. Moreover, DA (10 μM) treatment obviously induced the decrease in the production of GDNF/NGF and the increase in TNFα levels in primary cultured neurons, which were blocked by addition of β-asarone (βASA). We also demonstrated that DA stimulated the activation of ASK1/JNK1 pathway. and the addition of anti-TNFα antibody reversed the inactivation of Notch signaling, the downregulation of neurotrophins and synaptic loss.Conclusions: Overall, we suggested that DA stimulated abundant production and secretion of neuronal TNFα, which elicited progressive loss of neurotrophic factors, leading to cognitive disorder of MHE.