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.

[Effect of Lepidium meyenii (Maca) on neurotransmitter level and neuro-endocrine-immune network of deficiency-cold and deficiency-heat syndrome rats].

The aim of this paper was to study the effect of Lepidium meyenii(Maca) on cyclic nucleotides, neurotransmitter levels and hypothalamic-pituitary-adrenal axis and immunization of deficiency-cold and deficiency-heat syndrome rats, in order to explore the cold and hot medicinal properties of Maca. SD rats were divided into blank group, deficiency-cold syndrome group, Cinnamomi Cortex of deficiency-cold syndrome(30 g·kg~(-1)) group, high and low-dose Maca groups(2.4, 1.2 g·kg~(-1)), deficiency-heat syndrome group, Phellodendri Chinensis Cortex(PCC) of deficiency-heat syndrome(5 g·kg~(-1)), and high and low-dose Maca groups(2.4, 1.2 g·kg~(-1)). 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 the deficiency-cold and deficiency-heat model. The levels of cAMP, cGMP, NE, DA, 5-HT, CRH, ACTH, CORT and IgM, IgG, C3, C4 were detected by radio immunoassay. Both the high-dose Maca group and the low-dose Maca group can significantly improve the overall state and body weight of rats with deficiency-cold syndrome(P<0.01, P<0.05), significantly increasing cAMP, cAMP/cGMP, NE, DA, ACTH(P<0.01, P<0.001), and significantly decreasing 5-HT(P<0.01, P<0.001). However, high-dose and low-dose Maca groups could not improve the deficiency-heat syndrome, and the levels of cAMP, cGMP, cAMP/cGMP, NE, DA, 5-HT and ACTH were not statistically significant. Maca had a significant regulatory effect on CORT, IgM, IgG and C3 content of rats with deficiency-cold and deficiency-heat syndrome(P<0.01, P<0.05, P<0.001). Maca showed the same effect with Cinnamomi Cortex in adjusting the levels of deficiency-cold rats, but in opposition to Phellodendri Chinese Cortex. This paper confirmed that Maca was slightly warm based on its effect on cyclic nucleotide levels and neuro-endocrine-immune networks by the pharmacological experimental method.

[Severe sepsis as an initial presentation in children with Wernicke' s encephalopathy: report of a case and literature review].

OBJECTIVE: Wernicke's encephalopathy (WE) is an acute neuropsychiatric syndrome resulting from thiamine deficiency, which is associated with significant morbidity and mortality. The disorder is still greatly underdiagnosed in children because of either a relatively non-specific clinical presentation in some cases or unrecognized clinical setting. The aim of this literature review was to provide knowledge of pediatric WE in an effort to assist in early diagnosis, thereby reducing the morbidity and mortality. METHODS: The clinical manifestations, characteristic magnetic resonance imaging (MRI), diagnosis and treatment of one case and the other 35 cases reported in the last decade in children were summarized. RESULTS: Thirty-six cases (22 boys and 14 girls, 2-month to 16-year-old) were analyzed. All the other 35 cases except for our case had underlying diseases: improper feeding in 25/35 cases, long-time vomiting in 5/35 cases, immunosuppressive therapy in 4/35 cases, long-time total parenteral nutrition without multivitamin preparations supplementation in 3/35 cases and anorexia nervosa in 1/35 case. The classic triad (mental-status changes, nystagmus and ophthalmoplegia, and ataxia) was seen in 6/36 cases. The other clinical manifestations included consciousness disturbance in 24/36 cases, infection in 22/36 cases, pathological reflex and muscular tension changes in 18/36 cases, convulsion in 17/36 cases, developmental delay in 4/36 cases and failure to thrive in 2/36 cases. Cerebrospinal fluid examination was performed in 31/36 cases, and a slightly raised protein concentration was seen in 7/31 cases. The cerebrospinal fluid lactate levels were detected in 4/36 cases (all increased), serum lactic acid levels in 7/36 cases (6/7 cases increased), serum pyruvate in 4/36 cases (all increased), thiamine pyrophosphate effect (TPPE) in 9/36 cases (all increased), and serum thiamine in 2/36 cases (increased in 1/2 cases). The brain computed tomography (CT) scan was conducted in 20/36 cases and 16/20 cases showed abnormal hypodensity in bilateral basal ganglia, one case revealed diffuse cortical atrophy. The brain MR scan was conducted in 13/36 cases and all the 13 cases revealed symmetrical abnormal signal in bilateral mamillary body and basal ganglia, and 7/13 cases showed abnormal signals in the tegmentum of midbrain, cerebral aqueduct and white matter around the third and fourth ventricles. The diagnosis of WE was confirmed by MR in 12 cases, triad combined with MR in 3 cases, autopsy in 1 case among the 13 cases who underwent MR scan. The diagnosis of WE was confirmed by the TPPE and/or lactate levels in 9/11 cases. The initial thiamine was given by intravenous or intramuscular infusion in 33/36 cases, unknown method in 1 case, orally in 1 case and no thiamine was used in 1 case. The dosage of thiamine was 100 mg daily in 29/35 cases, unknown in 3/35 cases, 50 mg daily in 2/35 cases, 600 mg daily in 1/35 case. 34/35 patients' clinical symptoms improved during 24 hours to 1 week after initial treatment, and 1 case died due to no response to thiamine. Nineteen patients were followed up for 2-2.5 months and 17 cases recovered completely. CONCLUSION: Wernicke's encephalopathy can be difficult to diagnose because of a relatively non-specific clinical presentation. The characteristic MRI findings and the dramatic response of neurological signs to parenteral thiamine will assist early clinical diagnosis. Early and timely thiamine supplementation could reverse the clinical features and improve the prognosis in most cases.

[Effect of renshen jianxin capsule for alleviating insulin resistance in patients with coronary heart disease and glucose tolerance impairment].

OBJECTIVE: To explore the effect of Renshen Jianxin Capsule (RJC) on insulin resistance in patients with coronary heart disease (CHD) and glucose tolerance impairment (GTI). METHODS: Eighty patients with CHD-GTI of qi-deficiency blood-stasis syndrome were randomly assigned to 2 groups equally, the treated group was treated by RJC and the control group by metformin, based on the conventional Western medical treatment with nitric esters for 20 weeks. Changes before and after treatment in clinical symptoms and levels of blood glucose insulin, and insulin sensitivity index (ISI) were observed. RESULTS: The scores of clinical symptoms of Chinese medicine decreased in both groups, which showed statistical significances compared with those before treatment (P<0.01, P<0.05). On alleviating the angina pectoris, the markedly effective rate of the treated group is 47.5%, the total effective rate was 80.0%, and the difference between the two groups showed statistical significance (P<0.05). FBG, INS and ISI were improved significantly in both groups after treatment (P<0.05, P<0.01); while the three indices showed in significant difference between the two groups after treatment (P> 0.05). CONCLUSION: RJC was effective in improving insulin resistant, which may be one of the mechanisms of its therapeutic effect on CHD.

[Effects of tyrosine kinase receptor B and brain-derived neurotrophic factor on chemoresistance in neuroblastoma].

OBJECTIVE: Neuroblastoma (NB) is a pediatric solid tumor derived from neural crest precursor cells. It is resistant to current therapeutic protocols, including high dose chemotherapy. The mechanisms of chemoresistance are very complex. The recent studies have shown that the levels of tyrosine kinase receptor B (TrkB) and brain-derived neurotrophic factor (BDNF) are high in NB tumors with poor prognosis. The aim of this research was to explore the effects of TrkB and BDNF levels on the chemotherapeutic sensitivity in neuroblastoma by using the NB cell line SH-SY5Y in vitro. METHODS: The expression of TrkB protein was detected with Western-blot after the treatment with different concentrations of all trans-retinoic acid (ATRA). Cell survival rate was analyzed using MTT. Apoptosis was detected using flow cytometry (FCM) and a transmission electron microscope (TEM). RESULTS: (1) The expression of TrkB protein was undetectable in SY5Y. It was positive, however, after the treatment with ATRA (1, 10, 100 nmol/L) for five days. The level of TrkB protein was increased with adding of ATRA at different concentrations. (2) The difference of the survival and apoptotic rate between the BDNF (10 ng/ml) + ATRA (10 nmol/L) + cisplatin (CP, 5 microg/ml) group (survival rate 46.51% +/- 13.44%, apoptosis rate 11.79% +/- 1.53%) and the CP alone group (survival rate 38.51% +/- 9.66%, apoptosis rate 14.95% +/- 2.06%) was not statistically significant (P > 0.05). The survival rate of the BDNF (50 ng/ml and 100 ng/ml) + ATRA (10 nmol/L) + CP (5 microg/ml) group (66.85% +/- 18.39%, 94.30% +/- 10.71%) was greatly higher than CP alone group (P < 0.05, P < 0.01), whereas the apoptotic rate (9.36% +/- 1.03%, 5.20% +/- 1.99%) was significantly lower than that of the CP alone group (P < 0.01, P < 0.01). The survival rates of BDNF (100 ng/ml) + ATRA (10 nmol/L) + CP (5 microg/ml) group were higher than those of BDNF (50 ng/ml) + ATRA (10 nmol/L) + CP (5 microg/ml) group (P < 0.01), whereas the apoptotic rates were lower than those of BDNF (50 ng/ml) + ATRA (10 nmol/L) + CP (5 microg/ml) group (P < 0.05). There were no significant difference between the ATRA (1 nmol/L) + BDNF (50 ng/ml) + CP group (survival rate 45.33% +/- 11.83%, apoptosis rate 12.48% +/- 2.48%) and the CP alone group in the survival and apoptotic rates (P > 0.05). The survival rates of the ATRA (10 nmol/L, 100 nmol/L) + BDNF (50 ng/ml) + CP (61.62% +/- 18.53%, 105.02% +/- 5.55%) group were greatly higher than those of the CP alone group (P < 0.05, P < 0.01), whereas the apoptotic rate (9.36% +/- 1.03%, 5.05% +/- 1.88%) was significantly lower than that of the CDDP alone group (P < 0.05, P < 0.01). The survival rates of the ATRA (100 nmol/L) + BDNF (50 ng/ml) + CP group were higher than those of the ATRA (10 nmol/L) + BDNF (50 ng/ml) + CP group (P < 0.01), whereas the apoptotic rates were lower than the ATRA (10 nmol/L) + BDNF (50 ng/ml) + CP group (P < 0.01). (3) Some of the cells showed apoptotic changes in the CP alone group, whereas the intranuclear chromoplasma was well-distributed, the nuclear membrane was clear, and mitochondria, ribosome and solvent were present in the ATRA (10 nmol/L) + BDNF (50 ng/ml) + CP group. CONCLUSIONS: The sensitivity of SY5Y to CP was affected by TrkB and BDNF. The higher the level of TrkB and BDNF was, the lower the sensitivity of SY5Y to CP.

[The changes of three endogenous hormones during flower bud differentiation of Schisandga chinensis].

OBJECTIVE: To reveal the relation between endogenous hormones and the flower bud differentiation in Schisandga chinensis. METHOD: Top buds of extremely short branch and axillary buds of long branch in the same plant of S. chinensis were used as material and the contents of endogenous hormones were measured during different periods of the flower bud differentiation with HPLC. RESULT: The result showed that flower bud differentiation and the formation of female flower were inhibited by high concentration of GA3 and were promoted by high concentration of ABA or ZT. Low ratio of GA3/ABA has the same result. CONCLUSION: There was a correlation between endogenous hormones and the flower bud differentiation of S. chinensis.