ABSTRACT
Parkinson's disease （PD） is a progressive chronic neurodegenerative disorder with a complex pathogenesis involving oxidative stress， neuroinflammation， mitochondrial dysfunction， and other factors. Currently， the clinical treatment of PD mainly includes levodopa， dopamine receptor agonists， monoamine oxidase B inhibitors， catechol-O-methyltransferase inhibitors， and anticholinergic drugs， but there is a lack of disease-modif g therapies that can definitively improve disease progression. According to the understanding of traditional Chinese medicine （TCM）， PD is characterized by asthenia in origin and sthenia in superficiality. It is primarily caused by liver-kidney Yin deficiency， Qi-blood insufficiency， and closely related to wind， fire， phlegm， and blood stasis. Numerous clinical practices have shown that TCM has significant clinical value in the prevention and treatment of PD， the management of motor and non-motor symptoms， and the neuroprotection of dopaminergic neurons. The underlying mechanisms of TCM include antioxidative stress， anti-neuroinflammation， and regulation of mitochondrial dysfunction. This article categorized and summarized the pathogenesis of PD， systematically elucidated the pharmacological actions and molecular mechanisms of TCM monomer extracts and compounds in the prevention and treatment of PD， and provided the latest clinical research progress， aiming to provide references for the development and clinical use of TCM for PD.
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ObjectiveTo explore the mechanism of Dendrobium huoshanense polysaccharide （DHP） against inflammatory damage of neurons in Parkinson's disease （PD） model. MethodSH-SY5Y cells were randomized into blank group， model group， and DHP group. The survival rate of cells was measured by thiazole blue（MTT） assay， and the levels of lactate dehydrogenase （LDH）， reactive oxygen species （ROS）， malondialdehyde （MDA）， and superoxide dismutase （SOD） were measured by colorimetric analysis. BV-2 microglia were classified into blank group， model group， DHP group， and MCC950 group （positive control group）， and enzyme-linked immunosorbent assay （ELISA） was applied to detect the levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-18 （IL-18）. The expression of NOD-like receptor protein 3 （NLRP3）， adaptor protein apoptosis-associated dot protein （ASC）， cysteine aspartic protease-1 （Caspase-1）， and IL-1β was measured by Western blot. A total of 50 C57BL/6 mice were randomized into blank group， model group， DHP low-dose （100 mg·kg-1） group， DHP equivalent-dose （350 mg·kg-1） group， and MCC950 group （positive control group）， 10 mice in each group. The motor balance and coordination of C57BL/6 mice were observed by beam walking test， tail suspension test and rotarod test. The levels of Iba-1 and tyrosine hydroxylase （TH） were detected by immunofluorescence staining. The damage of dopaminergic neurons in the substantia nigra was detected by FJB staining. The levels of inflammatory factors such as IL-1β， IL-18， and TNF-α in mouse midbrain tissues were detected by ELISA and the protein levels of NLRP3， ASC， Caspase-1， and IL-1β protein were measured by Western blot. ResultCompared with the blank group， the SH-SY5Y model group showed decreased cell survival， increased levels of LDH， ROS， and MDA （P<0.05）， and decreased levels of SOD （P<0.05）. Compared with the model group， the DHP group demonstrated increased cell survival， decreased levels of LDH， ROS， and MDA （P<0.01）， and increased level of SOD （P<0.01）. Compared with the blank group， BV-2 model group had high levels of IL-1β， IL-18， and TNF-α （P<0.05） and high protein expression of NLRP3， Caspase-1， IL-1β， and ASC （P<0.05）. Compared with the model group， DHP and MCC950 groups demonstrated low levels of IL-1β， IL-18， and TNF-α （P<0.01） and low protein expression of NLRP3， Caspase-1， IL-1β， and ASC （P<0.01）. Compared with the blank group， the C57BL/6 model group displayed long time to pass the balance wood （P<0.05）， short time spent on the rod in the rotarod test （P<0.05）， high levels of IL-1β， IL-18， and TNF-α （P<0.05） and expression of Iba-1 in the midbrain substantia nigra （P<0.05）， low TH expression （P<0.05）， more positive neurons in the FJB staining （P<0.05）， and high expression of NLRP3， Caspase-1， ASC， and IL-1β proteins （P < 0.05）. Compared with the model group， the mice in the DHP and MCC950 groups had short time to pass the balance beam （P<0.01）， long time spent on the rod （P<0.01）， low levels of IL-1β， IL-18， and TNF-α （P<0.01）， low Iba-1 expression in midbrain substantia nigra （P<0.01）， high TH expression （P<0.01）， and small number of positive neurons in the midbrain substantia nigra （P<0.01）. The expression of NLRP3， ASC， and IL-1β proteins was lower in the MCC950 group （P<0.01）， and the expression of NLRP3， ASC， Caspase-1 and IL-1β proteins was lower in the DHP equivalent-dose group （P<0.01） than in the model group. ConclusionDHP has anti-oxidative stress effect. It regulates the expression of NLRP3 inflammasome and inhibits the overactivation of microglia， thereby alleviating the neuroinflammatory injury in PD and exerting the neuroprotective effect.
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Objective To observe the effect of plasma exchange (PE)therapy for removing serum interleukin-6 (IL-6),tumor necrosis factor alpha (TNFα),and interferon gamma (IFNγ)in patients with liver failure,and to assess the value of artificial liver support system in the treatment of liver failure.Methods The study included 36 patients with liver failure who were hospitalized in the First Affiliated Hospi-tal of Bengbu Medical College from February 2012 to February 2013.Blood samples were collected before PE and the next morning after mul-tiple treatments.Plasma TNFα,IL-6,and IFNγlevels were measured by ELISA.Between-group comparison of measurement data before and after treatment was made by independent-samples t test,and comparison of mean values between groups was made by analysis of vari-ance.Results All the 36 liver failure patients had significantly lower levels of TNFα(381.23 ±190.57 ng/L vs 274.12 ±212.30 ng/L,P0.05).After PE therapy,29 out of 36 liver failure patients recovered well,while the remaining 7 patients deteriorated.The recovered group had significantly greater decreases in TNFα(122.58 ±57.64 ng/L vs 42.45 ±19.86 ng/L,P<0.05),IL-6 (26.93 ±7.25 ng/L vs 6.71 ±3.55 ng/L,P<0.05),and IFNγ(284.06 ±94.31 ng/L vs 217.47 ±45.76 ng/L,P<0.05)than the deteriorated group.The response rates of patients with acute,subacute,acute -on -chronic,and chronic liver failure were 66.67%,85.71%,86.36%,and 50%,respectively.Conclusion Continuous artificial liver PE therapy can effectively remove pro-inflammatory cytokines from plasma and thus improve the clinical outcomes of patients with liver failure.
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Objective To evaluate the association between parameters of heart rate turbulence (HRT) and the severity of the coronary arteries disease. Methods 60 patients with unstable angina pectoris (UAP) who under-went angiographic examination and 40 healthy controls were chosen. HRT including turbulence onset (TO), turbu-lence slope (TS) and turbulence dynamicity (TD) were determined by 24 h ambulatory electrocardiogram(Hoher) in all the patients. The value of above indices were compared between UAP group and control group,and between subgroups of UAP. The correlation of HRT with the severity of coronary arteries diseases was analyzed. Results The levels of TO and TD in patients with UAP were significantly higher than those in controls [(1.18±0.88) % vs lower TS (P<0.05) and higher TD (P<0.05 ) than those in patients with coronary single vessel lesion. The same -0.296, P<0.05 ) and coronary artery stenosis score (r=-0.372, P<0.05 ) ; TD was positively correlated with number of abnormal coronary artery (r=0.353, P<0.01 ) and coronary artery stenosis score (r=0.510, P < 0.05). Conclusion . HRT is impaired in patients with UAP,especially the changes of TS and TD is signflcant,and is correlated with the severity of coronary arteries disease. TD is not influenced by premature ventricualr contractionheart rate so the combinatoin of TD and TS might be used as objective index in predicting the severity of the coronary arteries disease.