Current Issue : April - June Volume : 2018 Issue Number : 2 Articles : 5 Articles
Danhong injection (DHI) has been widely used in China for cardiocerebrovascular diseases treatments. And in this study, we\ndemonstrated the therapeutic effect ofDHI on experimental diabetic neuropathy for the first time. Methods. Streptozotocin- (STZ-)\ninduced SD rats were used. In experiment 1, 4-week treatment with DHI or saline started 4 weeks after STZ injection; mechanical\nallodynia was measured before and every 2 weeks after STZ injection. In experiment 2, chronic intrathecal infusion of U0126 was\nconducted during the 8th week of diabetes. Phosphorylated and total ERK1/2 in spinal cord were analyzed by western blot. BDNF\nlevel in sciatic nerve was evaluated by ELISA. Results. DHI treatment significantly alleviated mechanical allodynia at the end of\nthe study and downregulated the expression of phosphorylated ERK1/2 in spinal cord. In addition, DHI treatment also elevated\nbrain-derived neurotrophic factor (BDNF) level in sciatic nerve of DPN rat. In experiment 2, inhibition of ERK1/2 activation\nwas confirmed to result in the alleviation of mechanical allodynia. Conclusions. We demonstrated that DHI was able to alleviate\nmechanical allodynia in diabetic neuropathy rat through inhibiting the activation of ERK1/2. The reduction of BDNF content in\nsciatic nerve was also partially reversed by DHI treatment....
Matrine may be protective against colorectal cancer (CRC), but how it may work is unclear. Thus, we explored the underlying\nmechanisms of matrine in CRC. Matrine-related proteins and CRC-related genes and therapeutic targets of matrine in CRC\nwere predicted using a network pharmacology approach. Five targets, including interleukin 6 (IL-6), the 26S proteasome, tumor\nnecrosis factor alpha (TNF-�±), transforming growth factor beta 1 (TGF-�²1) and p53, and corresponding high-mobility group\nbox 1 (HMGB1) signaling and T helper cell differentiation were thought to be associated with matrineâ��s mechanism. Expression\nof predicted serum targets were verified in a 1,2-dimethylhydrazine dihydrochloride-induced CRC model rats that were treated\nwith matrine (ip) for 18 weeks. Data show that matrine suppressed CRC growth and decreased previously elevated expression of\nIL-6, TNF-�±, p53, and HMGB1. Matrine may have had a therapeutic effect on CRC via inhibition of HMGB1 signaling, and this\noccurred through downregulation of IL-6, TNF-�±, and HMGB1....
This study aimed to evaluate the clinical analgesic efficacy and identify the molecular targets of XGDP for treating primary\ndysmenorrhea (PD) by a network pharmacology approach. Analysis of pain disappearance rate of XGDP in PD treatment was\nconducted based on data from phase II and III randomized, double-blind, double-simulation, and positive parallel controlled\nclinical trials. The bioactive compounds were obtained by the absorption, distribution, metabolism, and excretion processes with\noral bioavailability (OB) and drug-likeness (DL) evaluation. Subsequently, target prediction, pathway identification, and network\nconstructionwere employed to clarify the mechanisms of the analgesic effect of XGDP on PD.Thepain disappearance rates in phase\nII and III clinical trials of XGDP in PD treatment were 62.5% and 55.8%, respectively, yielding a significant difference (...
Alzheimerââ?¬â?¢s disease (AD) is a neurodegenerative disorder responsible for the majority of dementia cases in elderly people. It is\nwidely accepted that the main hallmarks of AD are not only senile plaques and neurofibrillary tangles but also reactive\nastrogliosis, which often precedes detrimental deposits and neuronal atrophy. Such phenomenon facilitates the regeneration of\nneural networks; however, under some circumstances, like in AD, reactive astrogliosis is detrimental, depriving neurons of the\nhomeostatic support, thus contributing to neuronal loss. We investigated the presence of reactive astrogliosis in 3Ã?â??Tg-AD mice\nand the effects of palmitoylethanolamide (PEA), a well-documented anti-inflammatory molecule, by in vitro and in vivo studies.\nIn vitro results revealed a basal reactive state in primary cortical 3Ã?â??Tg-AD-derived astrocytes and the ability of PEA to\ncounteract such phenomenon and improve viability of 3Ã?â??Tg-AD-derived neurons. In vivo observations, performed using\nultramicronized- (um-) PEA, a formulation endowed with best bioavailability, confirmed the efficacy of this compound.\nMoreover, the schedule of treatment, mimicking the clinic use (chronic daily administration), revealed its beneficial\npharmacological properties in dampening reactive astrogliosis and promoting the glial neurosupportive function. Collectively,\nour results encourage further investigation on PEA effects, suggesting it as an alternative or adjunct treatment approach for\ninnovative AD therapy....
Parkinson�s disease (PD) was one of the most common neurodegenerative diseases with a slow and progressive loss of dopamine\n(DA) neurons in the midbrain substantia nigra (SN). Neuroinflammation was identified to be an important contributor to PD\npathogenesis with the hallmark of microglia activation. Tetrahydroxystilbene glucoside (TSG) was the main active component\nextracted from Polygonum multiflorum and held amounts of pharmacological activities including antioxidant, free radicalscavenging,\nanti-inflammation, and cardioprotective properties. Recent studies demonstrated that TSG exerted neuroprotection\nfrom several neurodegenerative disease models. However, the underlying mechanisms were not completely elucidated. In the\npresent study, rat nigral stereotaxic injection of 6-hydroxydopamine- (6-OHDA-) elicited DA neuronal injury was performed to\ninvestigate TSG-mediated neuroprotection on DA neurons. In addition, primary rat midbrain neuron-glia cocultures were\napplied to explore the mechanisms underlying TSG-exerted neuroprotection. Results showed that daily intraperitoneal injection\nof TSG for 14 consecutive days significantly protected DA neurons from 6-OHDA-induced neurotoxicity and suppressed\nmicroglia activation. Similar neuroprotection was shown in primary neuron-glia cocultures. In vitro studies further\ndemonstrated that TSG inhibited microglia activation and subsequent release of proinflammatory factors. Moreover, TSGmediated\nneuroprotection was closely related with the inactivation of mitogen-activated protein kinase (MAPK) signaling\npathway. Together, TSG protects DA neurons from 6-OHDA-induced neurotoxicity via the inhibition of microglia-elicited\nneuroinflammation. These findings suggest that TSG might hold potential therapeutic effects on PD....
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