[Anti-fatigue effect of Lubian on kidney Yin deficiency and kidney Yang deficiency mice and mechanism based on PI3K-Akt pathway].

This study aimed to investigate the anti-fatigue effect and mechanism of Lubian(Cervi Penis et Testis) on kidney Yin deficiency and kidney Yang deficiency mice. After one week of adaptive feeding, 88 healthy male Kunming mice were randomly divided into a blank group, a kidney Yin deficiency model group, a kidney Yin deficiency-Panacis Quinquefolii Radix(PQR) group, kidney Yin deficiency-Lubian treatment groups, a kidney Yang deficiency model group, a kidney Yang deficiency-Ginseng Radix et Rhizoma(GR) group, and kidney Yang deficiency-Lubian treatment groups, with eight mice in each group. The kidney Yin deficiency model and kidney Yang deficiency model were prepared by daily regular oral administration of dexamethasone acetate and hydrocortisone, respectively, and meanwhile, corresponding drugs were provided. The mice in the blank group received blank reagent. The treatment lasted 14 days. The exhaustive swimming time was measured 30 min after drug administration on the 14th day. On the 15th day, blood was collected from eyeballs and the serum was separated to determine the content of lactic acid(LD), blood urea nitrogen(BUN), lactate dehydrogenase(LDH), cyclic adenosine monophosphate(cAMP), and cyclic guanosine monophosphate(cGMP). The liver was dissected to determine the content of liver glycogen and the protein expression of phosphoinositide 3-kinase(PI3K) and protein kinase B(Akt). Compared with the kidney Yang deficiency model group, the kidney Yang deficiency-Lubian treatment groups showed increased body weight(P<0.05), relieved symptoms of Yang deficiency, decreased cGMP content(P<0.01), increased cAMP/cGMP(P<0.01), prolonged exhausted swimming time(P<0.01), reduced LD(P<0.01), elevated BUN content(P<0.01), increased liver glycogen content(P<0.01), and increased protein expression of PI3K and Akt in the liver(P<0.05). Compared with the kidney Yin deficiency model group, the kidney Yin deficiency-Lubian treatment groups showed increased body weight(P<0.01), relieved symptoms of Yin deficiency, increased content of cGMP(P<0.01), decreased cAMP/cGMP(P<0.01), prolonged exhausted swimming time(P<0.01), decreased LD(P<0.01), decreased BUN content(P<0.01), increased liver glycogen content(P<0.01), and increased protein expression of PI3K(P<0.05) and Akt in the liver(P<0.05). To sum up, Lubian can regulate Yin deficiency and Yang deficiency and increase glycogen synthesis by affecting the PI3K-Akt pathway, thereby exerting an anti-fatigue role.

[Construction of a high-throughput screening model for mitochondrial function of Aconiti Lateralis Radix Praeparata by machine learning algorithm and mechanism analysis].

A high-throughput screening machine learning model for mitochondrial function was constructed, and compounds of Aco-niti Lateralis Radix Praeparata were predicted. Deoxyaconitine with the highest score and benzoylmesaconine with the lowest score among the compounds screened by the model were selected for mitochondrial mechanism analysis. Mitochondrial function data were collected from PubChem and Tox21 databases. Random forest and gradient boosted decision tree algorithms were separately used for mo-deling, and ECFP4(extended connectivity fingerprint, up to four bonds) and Mordred descriptors were employed for training, respectively. Cross-validation test was carried out, and balanced accuracy(BA) and overall accuracy were determined to evaluate the performance of different combinations of models and obtain the optimal algorithm and hyperparameters for modeling. The data of Aconiti Lateralis Radix Praeparata compounds in TCMSP database were collected, and after prediction and screening by the constructed high-throughput screening machine learning model, deoxyaconitine and benzoylmesaconine were selected to measure mitochondrial membrane potential, reactive oxygen species(ROS) level and protein expression of B-cell lymphoma 2(Bcl-2), Bcl-2-associated X protein(Bax) and peroxisome proliferator-activated receptor-γ-coactivator 1α(PGC-1α). The results showed that the model constructed using gradient boosted decision tree+Mordred algorithm performed better, with a cross-validation BA of 0.825 and a test set accuracy of 0.811. Deoxyaconitine and benzoylmesaconine changed the ROS level(P<0.001), mitochondrial membrane potential(P<0.001), and protein expression of Bcl-2(P<0.001, P<0.01) and Bax(P<0.001), and deoxyaconitine increased the expression of PGC-1α protein(P<0.01). The high-throughput screening model for mitochondrial function constructed by gradient boosted decision tree+Mordred algorithm was more accurate than that by random forest+ECFP4 algorithm, which could be used to build an algorithm model for subsequent research. Deoxyaconitine and benzoylmesaconine affected mitochondrial function. However, deoxyaconitine with higher score also affected mitochondrial biosynthesis by regulating PGC-1α protein.

Sodium Butyrate Exacerbates Parkinson's Disease by Aggravating Neuroinflammation and Colonic Inflammation in MPTP-Induced Mice Model.

The abnormal production of short chain fatty acid (SCFAs) caused by gut microbial dysbiosis plays an important role in the pathogenesis and progression of Parkinson's disease (PD). This study sought to evaluate how butyrate, one of SCFAs, affect the pathology in a subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine hydrochloride (MPTP) treated mouse model of PD. Sodium butyrate (NaB; 165 mg/kg/day i.g., 7 days) was administrated from the day after the last MPTP injection. Interestingly, NaB significantly aggravated MPTP-induced motor dysfunction (P < 0.01), decreased dopamine (P < 0.05) and 5-HT (P < 0.05) levels, exacerbated declines of dopaminergic neurons (34%, P < 0.05) and downregulated expression of tyrosine hydroxylase (TH, 47%, P < 0.05), potentiated glia-mediated neuroinflammation by increasing the number of microglia (17%, P < 0.05) and activating astrocytes (28%, P < 0.01). In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1ß, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells. In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice. However, NaB had no effect on NFκB, MyD88 and TNF-α expression in PD mice. Our results indicate that NaB exacerbates MPTP-induced PD by aggravating neuroinflammation and colonic inflammation independently of the NFκB/MyD88/TNF-α signaling pathway.

Neuroprotective effects of fecal microbiota transplantation on MPTP-induced Parkinson's disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway.

Parkinson's disease (PD) patients display alterations in gut microbiota composition. However, mechanism between gut microbial dysbiosis and pathogenesis of PD remains unexplored, and no recognized therapies are available to halt or slow progression of PD. Here we identified that gut microbiota from PD mice induced motor impairment and striatal neurotransmitter decrease on normal mice. Sequencing of 16S rRNA revealed that phylum Firmicutes and order Clostridiales decreased, while phylum Proteobacteria, order Turicibacterales and Enterobacteriales increased in fecal samples of PD mice, along with increased fecal short-chain fatty acids (SCFAs). Remarkably, fecal microbiota transplantation (FMT) reduced gut microbial dysbiosis, decreased fecal SCFAs, alleviated physical impairment, and increased striatal DA and 5-HT content of PD mice. Further, FMT reduced the activation of microglia and astrocytes in the substantia nigra, and reduced expression of TLR4/TNF-α signaling pathway components in gut and brain. Our study demonstrates that gut microbial dysbiosis is involved in PD pathogenesis, and FMT can protect PD mice by suppressing neuroinflammation and reducing TLR4/TNF-α signaling.

Neuroprotective Effects of Loganin on MPTP-Induced Parkinson's Disease Mice: Neurochemistry, Glial Reaction and Autophagy Studies.

Parkinson's disease (PD) is a progressive neurodegenerative disease, involving resting tremor and bradykinesia, for which no recognized therapies or drugs are available to halt or slow progression. In recent years, natural botanic products have been considered relatively safe, with limited side effects, and are expected to become an important source for clinical mediation of PD in the future. Our study focuses on the ability of loganin, a compound derived from fruits of cornus, to mediate neuroprotection in a mouse model of PD. Mice were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) with a dosage of 30 mg/kg daily for 5 days to establish a subacute PD model and treated with loganin. Locomotor activity was assessed by a pole test, then mice were euthanized at 1 and 3 days after the last treatment, and brain tissue was prepared for subsequent assays. Loganin rescued decrease of dopamine levels and tyrosine hydroxylase (TH) expression in the striatum, and shortened total locomotor activity (TLA) time of mice. Furthermore, loganin alleviated microglia and astrocyte activation, and suppressed TNF-α and caspase-3 expression through a c-Abl-p38-NFκB pathway. Loganin also downregulated LC3-II and Drp1 expression, and decreased the level of acidic vesicular organelles (AVOs). Loganin exerts neuroprotective effects on MPTP-induced PD mice by decreasing inflammation, autophagy, and apoptosis, suggesting that loganin could serve as a therapeutic drug to ameliorate PD. J. Cell. Biochem. 118: 3495-3510, 2017. © 2017 Wiley Periodicals, Inc.

Intradiencephalon injection of histamine inhibited the recovery of locomotor function of spinal cord injured zebrafish.

Human spinal cord injury (SCI) usually causes irreversible disability beneath the injured site due to poor neural regeneration. On the contrary, zebrafish show significant regenerative ability after SCI, thus is usually worked as an animal model for studying neuroregeneration. Most of the previous SCI studies focused on the local site of SCI, the supraspinal-derived signals were rarely mentioned. Here we showed that intradiencephalon injection of histamine (HA) inhibited the locomotor recovery in adult zebrafish post-SCI. Immunofluorescence results showed that intradiencephalon HA administration increased the activated microglia 3 days post injury (dpi), promoted the proliferation of radial glial cells at 7 dpi and affected the morphology of radial glial cells at 11 dpi. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR) results showed that intradiencephalon HA administration also reduced the expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF) and insulin-like growth factor1 (IGF-1) at the lesion site, however, had no effect on the expression of pro-inflammatory factors such as TNF-alpha and IL-1 beta. Hence, our data suggested that exogenous intradiencephalon HA retarded locomotor recovery in spinal cord injured zebrafish via modulating the repair microenvironment.

Copper-catalyzed chalcogenation of imidazoheterocycles with sulfur/selenium powder and coumarinyl triflates.

An efficient and convenient copper-catalyzed chalcogenation of imidazoheterocycles with sulfur/selenium powder and coumarinyl triflates has been described. This procedure provides a wide range of structurally diverse coumarinylthio-/coumarinylseleno-substituted imidazoheterocycles in good yields and with good functional group tolerance. Biological evaluation showed that the newly synthesized compound 6d possesses significant in vitro antiproliferative activities against human-derived esophageal, breast, stomach, and prostate cancer cell lines compared with the positive control, 5-fluorouracil.

[Effect of AÇaí (Euterpe oleracea) on lipid metabolism, immune substances and endocrine hormone in rats with deficiency-heat and deficiency-cold syndrome].

To study the effects of AÇaí(Euterpe oleracea) on lipid metabolism, immune substances and endocrine hormone level in rats with deficiency-heat and deficiency-cold syndrome. SD rats were divided into blank control group, deficiency-heat model group, deficiency-heat & Phellodendri Cortex group, deficiency-heat & AÇaí high dose and low dose groups, deficiency-cold model group, deficiency-cold & Cinnamomi Cortex group, deficiency-cold & AÇaí high dose and low dose groups. The rats received intramuscular injection of dexamethasone sodium phosphate (0.35 mg) or hydrocortisone sodium succinate (20 mg) for 21 days to set up deficiency-heat models and deficiency-cold models. Then the changes in fatmetabolism levels (FFA, LPL, HL) and immune indexes (IgG, IgM, C3 and C4) were detected by colorimeter; and the levels of endocrine hormone indexes (CORT, E2 and T) were detected by radioimmunoassay. The levels of FFA, LPL and HL in serum were reduced (P<0.01 or P<0.001); levels of IgG, IgM and C3 in serum were increased (P<0.05 or P<0.001); level of CORT in serum was increased (P<0.05) and the level of E2, E2/T in serum were reduced in the AÇaí high dose group (P<0.05). The effect of high dose AÇaí on fat metabolism was not obvious in deficiency-cold models, but the levels of IgG, IgM, C3 and CORT in serum were increased (P<0.05 or P<0.001). AÇaí was showed the same effect trend with Phellodendri Cortex in adjusting the levels of deficiency-heat rats; but unlike Cinnamomi Cortex, AÇaí was showed no obvious effect in adjusting the levels of deficiency-cold rats. In this experiment, homogeneous comparison and heterogeneous disproof were used to verify the cold nature of Çaí.

[Effects of Shaoyao Gancao decoction on contents of amino acids and expressions of receptors in brains of spastic paralysis rats].

To explore the effects of Shaoyao Gancao decoction on contents of amino acids and expressions of receptors in the brains of spastic paralysis rats, the spastic paralysis rat models of stroke convalescence were made by line tethering method. Baclofen was used as the control group, and the experiment group received Shaoyao Gancao decoction at 3∶1 proportions. After 3 weeks, the neurobehavioral scores, muscular tension and pain threshold were measured and compared. High performance liquid chromatography (HPLC) was used to detect the contents of GABA, Gly, Glu, Asp in cerebral cortex. The protein expressions of GABA receptors Aα1, B； NMDA receptor NR1, NR2A and NR2B in cerebral cortex were determined by immunohistochemistry assay. The results showed that the Shaoyao Gancao decoction at 3∶1 proportion could improve the spastic paralysis state after stroke, significantly improve neurological symptoms (P<0.01), decrease muscular tension (P<0.01) and improve pain threshold (P<0.05) as compared with model group. Simultaneously, the contents of inhibitory amino acids GABA and Gly were increased significantly (P<0.01), while with a decrease tendency in excitatory amino acids Glu and Asp (with no statistical significance). In addition, it could significantly increase the protein expressions of neurotransmitter GABA receptors Aα1, and B (P<0.05); reduce the expressions of neurotransmitter NMDA receptors NR1, NR2A and NR2B (P<0.05). These results suggested that the Shaoyao Gancao decoction at 3：1 proportion could effectively relieve spasm and pain. The mechanism might be associated with increasing the contents of inhibitory amino acids and increasing the expressions of their receptors in spastic paralysis rats after stroke, which would consequently enhance the signal transduction of inhibitory amino acids. Meanwhile, there was a decrease tendency in excitatory amino acids, although no significant effect was observed, and it could suppress the expressions of excitatory amino acids receptors, thus weaken the excitatory signal transduction. Thereby the neurotoxicity was relieved eventually. These findings indicated that Shaoyao Gancao decoction could regulate the balance of neurotransmitter system to relieve the spasticity, and eventually achieve tendon tonifying and spasm relieving effect.

[Effect of Acaí (Euterpe oleracea) on biological expression characteristics of deficiency-heat and deficiency-cold rats].

To study the effects of Acaí on biological expression characteristics in rats with deficiency-heat and deficiency-cold syndromes, SD rats were divided into blank group, deficiency-heat model group, deficiency-heat+Phellodendri Chinensis Cortex group, deficiency-heat+Acaí high dose and low dose groups, deficiency-cold model group, deficiency-cold+Cinnamomi Cortex group, deficiency-cold+Acaí high dose and low dose groups. The rats were treated with intramuscular injection of hydrocortisone (20 mg•kg⁻¹) or dexamethasone sodium phosphate (0.35 mg•kg⁻¹) for 21 days to set up deficiency-heat model and deficiency-cold models. The levels of cAMP, cGMP, T3, T4 and rT3 were detected by radioimmunoassay. The levels of TP, UA, TC, TG and ALB were detected by colorimetry. The level of cAMP, cAMP/cGMP in serum were reduced in Acaí high dose group (P<0.05, P<0.001). The levels of T3, T4 and rT3 were significantly reduced in the Acaí high dose group (P<0.01, P<0.001, P<0.05). The levels of TP, UA, TC, TG and ALB were significantly reduced in the Acaí high dose group (P<0.001, P<0.05, P<0.05, P<0.05, P<0.01). However, Acaí had no obvious effects on deficiency-cold models. Acaí showed the same effect with Phellodendri Chinensis Cortex in adjusting the levels of deficiency-heat rats; but unlike Cinnamomi Cortex, Acaí showed no obvious effects in adjusting the levels of deficiency-cold rats.

[Understanding and development strategy of health food containing Chinese materia medica].

Health food containing Chinese materia medica (CMM) conforms to the development demands of the age of big health and the theory of preventive treatment. In the view of health care and improvement of resisting diseases, it plays an important role in the market. It is very necessary to have further study and discussion on health food containing CMM. First of all, by comparing, analyzing and summarizing, the health food containing CMM could be defined as the health food which is qualified in security and functionality evaluation, with the traditional Chinese medicines(TCM) within TCM standards as the main raw materials, and the formulation-composition is based on the theory of TCM. It is characterized by higher safety than medicines, stronger biological activities than common food, multiple forms, abundant raw materials and integrated supervision and management. Secondly, we discussed the research and development (R&D) strategies and rules of health food containing CMM, pointing out that the core tasks of R&D include the investigation of formula, technology and the standards of quality. The fundamental principles of declaration and production include scientificity, rationality, reality and uniformity. Three key requirements (security, functionality and controllability) in the review as well as the process management of R&D and the key-points of risks control were summarized in this paper. Finally, the dynamic trends of policies and regulations related to health food containing CMM were analyzed in the view of registration, recording, raw materials and functions, and then related suggestions were proposed. Therefore, this article will be helpful in overall understanding the health food containing CMM and play a guiding role for its research and development.

[Investigation of effects of albiflorin and paeoniflorin on hippocampal BDNF and NO in chronic restraint stress rats].

This paper aimed to investigate the antidepressant-like effects and the mechanism of the albiflorin, paeoniflorin on rats with chronic restraint stress model. Fluoxetine and Xiaoyao group served as the positive control, body weight, sucrose preference test and the open field behavioral experiment were measured, the levels of nitric oxide (NO) in hippocampus were detected by Greg colorimetric method. Furthermore, the levels of brain derived neurotrophic factor (BDNF) in hippocampus were detected by ELISA. Finally, the expressions of nNOS mRNA in hippocampus detected by RT-qPCR, the protein levels of nNOS and BDNF in hippocampus were detected by Western blot. Compared with the model group,the pass counts of paeoniflorin group(30 mg•kg⁻¹) and albiflorin group(30 mg•kg⁻¹) were obviously increased(P<0.05,P<0.01). Furthermore, compared with the model group,the levels of NO in paeoniflorin groups(30 mg•kg⁻¹ and 15 mg•kg⁻¹) and albiflorin groups(30 mg•kg⁻¹ and 15 mg•kg⁻¹) were all significantly decreased(P<0.05,P<0.01; P<0.05, P<0.05). BDNF levels of paeoniflorin group(30 mg•kg⁻¹) and albiflorin group(30 mg•kg⁻¹) were obviously increased(P<0.05). Finally, compared with the model group, the expressions of nNOS mRNA of paeoniflorin groups(30 mg•kg⁻¹ and 15 mg•kg⁻¹) (P<0.01, P<0.01) and albiflorin groups(30 mg•kg⁻¹) were significantly decreased(P<0.05). Compared with the model group, the protein exprsssions of BDNF of paeoniflorin group(30 mg•kg⁻¹) and albiflorin group(30 mg•kg⁻¹) were obviously increased(P<0.05). Albiflorin and paeoniflorin have the effects of smooth the liver and dispel stagnation, the mechanism has the relevant with adjusting and controlling the expression of NO and BDNF in hippocampus.

[Effect of Individualized Low-protein Diet Intervention on Renal Function of Patients with Chronic Kidney Disease].

OBJECTIVE: To investigate whether individualized low-protein diet intervention for patients with chronic kidney disease(CKD)could improve the general condition,slow the deterioration of renal function,and delay the time of entering dialysis. METHODS: Forty CKD inpatients between July 2011 and July 2012 were randomly given with normal or individualized low-protein diet for six months according to random number table after signing informed consent. The levels of urine protein and biochemical indexes of renal function were measured at baseline and at the end of dietary intervention for six months, respectively. RESULTS: The baseline urine protein level,renal function,and biochemical indexes were not significantly different between these two groups. The diastolic blood pressure,protein intake,blood urea nitrogen,uric acid, potassium, phosphorus, C-reaction protein,24-hour urea nitrogen,and urine protein after six months were significantly lower than those at baseline,that is,(101.70 ± 15.78)mmHg vs.(91.75 ±15.52) mmHg,(63.87 ± 24.70)g/d vs.(50.02 ± 14.07)g/d,(20.01 ± 7.69)mmol/L vs.(15.11 ± 4.90) mmol/L,(362.75 ± 84.56)Μmol/L vs.(302.20 ± 8.48)Μmol/L,(5.22 ± 0.75)mmol/L vs.(4.79±0.36) mmol/L,(2.07 ± 0.68) mmol/L vs.(1.57 ± 0.41) mmol/L,1.19 [0.65,4.17] mg/L vs. 0.74 [0.38,1.33] mg/L,70.6 [8.70,101.18] mmol/L vs. 16.93 [3.23,72.27] mmol/L,1.00 [0.30,1.00] g/d vs. 0.15 [0,0.83] g/d (all P<0.05),among which albumin and hemoglobin were significantly higher [(0.34 ± 0.07)g/L vs.(0.37 ± 0.05)g/L, (99.38 ± 21.89)g/L vs.(126.35 ± 14.11)g/L,respectively] in the individualized low-protein diet group. The difference was statistically significant (P<0.05). The most relevant for urine protein producing was prealbumin (r=0.924, P<0.05). The differences of blood urea nitrogen, potassium, sodium, calcium, phosphorus, 24-hour urea nitrogen, urine specific gravity, urine protein, and hemoglobin in six months in the individualized low-protein diet group were significantly better than those in the normal low protein-diet group (P<0.05). CONCLUSIONS: Individualized low-protein diet intervention may have definite curative effectiveness in CKD patients. It can markedly improve the patients' condition,slow down the deterio-ration of renal function,and increase serum prealbumin levels that may reduce the generation of urine protein. It is worthy of wider clinical application.

[Efficacy analysis and theoretical study on Chinese herbal properties of Açaí (Euterpe oleracea)].

Açaí (Euterpe oleracea) emerged as a source of herb has a long history in South America, which was approved by the Ministry of Health used in China and it has been introduced planting in Guangdong and Taiwan. This article summarized applied history of Açaí and its present status in China. Did theoretical study on the Chinese herbal properties of Açaí based on the Chinese traditional philosophical culture to analysis the function and symptom preliminary, combining with used for medical recordation, chemical component, biological activity. It is aiming at establishing the theoretical foundation for the application under the guidance of TCM theory.

[Comparative study on effects of blood enriching on mouse model of blood deficiency syndrome induced by cyclophosphamide of albiflorin, paeoniflorin on levels of GM-CSF, IL-3 and TNF-α].

OBJECTIVE: To compare the effects and mechanism of blood enriching on mouse model of blood deficiency syndrome induced by cyclophosphamide of albiflorin and paeoniflorin. METHOD: Albiflorin and paeoniflorin were determined by using animal models of blood deficiency syndrome induced by cyclophosphamide. The amount of WBC, RBC, HGB, index of thymus gland and spleen, and the changes of GM-CSF, IL-3 and TNF-α in serum were detected after the treatment. RESULT: Compared with the model group, the amount of WBC in the group of 30 mg x kg(-1) albiflorin and 30 mg x kg(-1) paeoniflorin were increased obviously (P < 0.01). The amount of RBC in the group of 30 mg x kg(-1) albiflorin and 30 mg x kg(-1) paeoniflorin were increased obviously (P < 0.01, P < 0.001), which did not had a significant difference compared with the same dose. The index of thymus gland in the group of 30 mg x kg(-1) albiflorin was superior to the model group (P < 0.01), the difference was significant compared with the same dose of paeoniflorin (P < 0.05). The GM-CSF in serum in all groups of 30 mg x kg(-1) albiflorin, 15 mg x kg(-1) albiflorin, 30 mg x kg(-1) paeoniflorin and 15 mg x kg(-1) paeoniflorin increased obviously (P < 0.01, P < 0.05, P < 0.01, P < 0.05); The IL-3 in serum in both group of 30 mg x kg(-1) albiflorin and 30 mg x kg(-1) paeoniflorin also increased (P < 0.001). The content of TNF-α in group of 30 mg x kg(-1) albiflorin and 30 mg x kg(-1) paeoniflorin were reduced (P < 0.01), which showed the obvious difference compared with the same dose group (P < 0.01). CONCLUSION: Albiflorin had the effect of blood enriching by regulating the immune function, same with the paeoniflorin. The probable mechanism of nourishing blood and liver of Paeoniae Radix Alba was not only the better effect of adjusting the content of TNF-α, but also might act synergistically with paeoniflorin.

[Protective effect of Acai berries on chronic alcoholic hepatic injury in rats and their effect on inflammatory cytokines].

OBJECTIVE: To study the protective effect of Acai berries(Euterpe oleraceae) on chronic alcoholic hepatic injury in rats and their mechanism. METHOD: Wistar rats were fed for 1 week and randomly divided into blank group, model group, Dongbao Gantai group, Acai 1.6, 0.8, 0.4 g . kg-1 groups. The blank group was given distilled water, and the other groups were orally given 56% white spirit (Erguotou) for eight weeks at the dosages of 8 mL . kg-1 in the 1st week, which increased by 0.1 mL week by week till to 15 mL . kg-1, in order to establish the chronic hepatic injury model, and observe the effect of Acai berry freeze-dried powder on hepatocyte membrane permeability, liver lipid peroxidation, changes in inflammatory cytokines and pathological changes in hepatocytes. RESULT: Acai berries could significantly reduce serum ALT and AST(P<0.05), MDA(P<0.05), TG(P<0.05) and serum TNF-α and IL-6(P <0.05) and increase GSH and SOD(P <0.05). According to liver histopathological observation, livers in the model group were dominated by steatosis, some livers suffered spotty necrosis and inflammatory cell infiltration; The positive drug and Acai groups showed different changes in pathologic changes in rat livers. CONCLUSION: Acai berries show s specific protective effect on alcoholic hepatic injury. Its mechanism may be correlated with the inhibition of such inflammatory factors as TNF-α and IL-6.

[Study on blood enriching effects of γ-ray radiation of paeoniflorin and albiflorin on mouse model of blood deficiency].

OBJECTIVE: To study the blood enriching effects of Paeoniae Radix Rubra and Paeoniae Radix Alba, paeoniflorin and albiflorin on mouse model of blood deficiency caused by γ-ray radiation. METHOD: Build mouse model of blood deficiency induced by γ-ray radiation. Paeoniae Radix Rubra and Paeoniae Radix Alba were given during modeling. The amount of WBC was detected af- ter the treatment. Based on the result of WBC and paeoniflorin content, albiflorin content in Paeoniae Radix Rubra and Paeoniae Radix Alba, the same model and the same method were used to comparatively study the effect of blood enriching of paeoniflorin and albiflorin. RESULT: On the 7th day, the amount of WBC in model mice treated with 2 g x kg(-1) Paeoniae Radix Alba and 2 g x kg(-1) Paeoniae Radix Rubra significantly increased compared with that of model group (P < 0.05). In another experiment with the same model, the amount of WBC in model mice treated with 120 mg x kg(-1) paeoflorin and 120 mg x kg(-1) albiflorin significantly increased (P < 0.05) compared with that of model group on the 7th day. On the 10th day, the amount of WBC in rats treated with 120 mg x kg(-1) paeoflorin increased significantly (P < 0.05) compared with that of model group. Compared with the same dose of paeoniflorin, the amount of WBC in mice treated with albiflorin had no significant difference. CONCLUSION: All Paeoniae Radix Alba, Paeoniae Radix Rubra, paeoniflorin and al- biflorin can raise the amount of WBC and have the effect of enriching blood induced by radiation, while paeoniflorin and albiflorin have a similar result in this model. The result indicated that both paeoniflorin and albiflorin are effective constituents in Paeoniae Radix Alba, and paeoniflorin work as the common effective constituent in both Paeoniae Radix Rubra and Paeoniae Radix Alba.

Immunomodulatory Effects of Lepidium meyenii Walp. Polysaccharides on an Immunosuppression Model Induced by Cyclophosphamide.

Background: Lepidium meyenii Walp. (Maca) has emerged as a functional plant food and traditional herb owing to its biological activities; Maca polysaccharides as an important active component of Maca have good immunomodulatory effect; however, studies on the immunomodulatory effect of Maca polysaccharides are mainly focused on macrophages; little attention has been devoted to the mechanisms and other immune cells. This study is aimed at investigating the immunomodulatory effects and mechanisms of Maca polysaccharides. Methods: Sixty mice were divided into five groups, and the mice were injected with cyclophosphamide to establish an immunosuppression model except for those in the common group. The body weights were measured, as well as immune-related indices, such as organ indices, haematological parameters, lymphocyte cycle, and proliferation, cytokine, and protein expression levels. Results: The weight loss and immune organ index decline caused by cyclophosphamide could be reversed by MP. Furthermore, MP increased WBC and HGB counts and reduced the ratio of G0/G1 phase obviously, increased the proportion of S phase and G2/M phase in peripheral blood lymphocytes, increased the counts of CD4+ T cells and the ratio of CD4+/CD8+, and reduced the inhibition rate of splenic lymphocytes. MP affected the production of cytokines by increasing IFN-γ, TNF-α, and IL-2 levels and by decreasing IL-4 levels. MP increased the mRNA expression of T-bet and the protein expression of Bcl-2 in the spleen and decreased the protein expression of caspase-3 and Bax. Conclusions: Maca polysaccharides might be the basic material for Maca's immunomodulatory effect. The mechanism was perhaps related to inhibiting lymphocyte apoptosis and promoting the balance of Th1/Th2 cell subsets.

Revealing the Common Mechanisms of Scutellarin in Angina Pectoris and Ischemic Stroke Treatment via a Network Pharmacology Approach.

OBJECTIVE: To investigate the shared mechanisms of scutellarin in angina pectoris (AP) and ischemic stroke (IS) treatment. METHODS: A network pharmacology approach was used to detect the potential mechanisms of scutellarin in AP and IS treatment by target prediction, protein-protein interaction (PPI) data collection, network construction, network analysis, and enrichment analysis. Furthermore, molecular docking simulation was employed to analyze the interaction between scutellarin and core targets. RESULTS: Two networks were established, including a disease-target network and a PPI network of scutellarin targets against AP and IS. Network analysis showed that 14 targets, namely, AKT1, VEGFA, JUN, ALB, MTOR, ESR1, MAPK8, HSP90AA1, NOS3, SERPINE1, FGA, F2, FOXO3, and STAT1, might be the therapeutic targets of scutellarin in AP and IS. Among them, NOS3 and F2 were recognized as the core targets. Additionally, molecular docking simulation confifirmed that scutellarin exhibited a relatively high potential for binding to the active sites of NOS3 and F2. Furthermore, enrichment analysis indicated that scutellarin might exert a therapeutic role in both AP and IS by regulating several important pathways, such as coagulation cascades, mitogen-activated protein kinase (MAPK) signaling pathway, phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, Toll-like receptor signaling pathway, hypoxia inducible factor-1 (HIF-1) signaling pathway, forkhead box O (FoxO) signaling pathway, tumor necrosis factor (TNF) signaling pathway, adipocytokine signaling pathway, insulin signaling pathway, insulin resistance, and estrogen signaling pathway. CONCLUSIONS: The shared underlying mechanisms of scutellarin on AP and IS treatment might be strongly associated with its vasorelaxant, anticoagulant, anti-inflammatory, and antioxidative effects as well as its effect on improving lipid metabolism.