Antioxidant and androgenic effects of dietary ginger on reproductive function of male diabetic rats

Abstract

This study evaluated the antioxidant and androgenic properties of ginger roots on the reproductive function of male diabetic rats. Animals were divided into three groups; the control (Control), diabetic (Diab) and diabetic fed with dietary ginger for 30?d (Diab?+?Z). Thereafter, blood samples were collected and reproductive organs (testis, epididymis, prostate and seminal vesicle) were removed for determination of sperm parameters, malondialdehyde (MDA) level, glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and aspartate and lactate aminotransferase (AST and ALT) activities. Dietary ginger decreased blood glucose and MDA level, increased reproductive organ weights and testosterone level, improved semen quantity and motility, and ameliorated the SOD, CAT and GPx activities as well as testis AST, ALT, LDH and ALP activities. Intake of ginger roots improves the antioxidant and androgenic reproductive function of male diabetic rats in addition to its antidiabetic property.     

Ginger extract modulates Pb-induced hepatic oxidative stress and expression of antioxidant gene transcripts in rat liver

Context: Spices and herbs are recognized sources of natural antioxidants that can protect from oxidative stress, thus play an important role in chemoprevention of liver diseases. Ginger is used worldwide primarily as a spicy condiment.

Objective: This study evaluated the ability of ginger extract (GE) to ameliorate oxidative-hepatic toxicity induced by lead acetate (PbAc) in rats.

Materials and methods: Five groups of animals were used: group I kept as control; groups II, IV, and V received PbAc (1?ppm in drinking water daily for 6 weeks, and kept for an additional 2 weeks without PbAc exposure); group III treated orally with GE (350?mg/kg body weight, 4?d per week) for 6 weeks; group IV (protective) received GE for 2 weeks before and simultaneously with PbAc; and group V (treatment) received GE for 2 weeks after PbAc exposure.

Results: GC-MS analysis of GE revealed its content of gingerol (7.09%), quercetin (3.20%), dl-limonene (0.96%), and zingiberene (0.18%). Treatment of PbAc-treated rats with GE has no effect on hepatic Pb concentrations. However, it maintained serum aspartate aminotransferase level, increased hepatic glutathione (157%), glutathione S-transferase (GST) (228%), glutathione peroxidase (GPx) (138%) and catalase (CAT) (112%) levels, and reduced hepatic malondialdehyde (80%). Co-treatment of PbAc group with GE upregulated mRNA expression of antioxidant genes: GST-α1 (1.4-fold), GPx1 (1.8-fold), and CAT (8-fold), while post-treatment with GE upregulated only mRNA expression of GPx1 (1.5-fold).

Conclusion: GE has an antioxidant protective efficacy against PbAc-induced hepatotoxicity, which appears more effective than its therapeutic application. However, the changes in antioxidant gene expression were not reflected at the protein level.     

6-Gingerol inhibits Vibrio cholerae-induced proinflammatory cytokines in intestinal epithelial cells via modulation of NF-κB

Context The effect of 6-gingerol (6G), the bioactive component of Zingiber officinale Roscoe (Zingiberaceae), in the reduction of Vibrio cholerae (Vibrionaceae)-induced inflammation has not yet been reported.

Materials and methods Cell viability assay was performed to determine the working concentration of 6G. Elisa and RT-PCR were performed with Int 407 cells treated with 50?μM 6G and 100 multiplicity of infection (MOI) V. cholerae for 0, 2, 3, 3.5, 6 and 8?h to determine the concentration of IL-8, IL-6, IL-1α and IL-1β in both protein and RNA levels. Furthermore, the effect of 50?μM 6G on upstream MAP-kinases and NF-κB signalling pathways was evaluated at 0, 10, 15, 30, 60 and 90?min.

Results The effective dose (ED₅₀) value of 6G was found to be 50?μM as determined by cell viability assay. Pre-treatment with 50?μM 6G reduced V. cholerae infection-triggered levels of IL-8, IL-6, IL-1α and IL-1β by 3.2-fold in the protein level and two-fold in the RNA level at 3.5?h. The levels of MAP-kinases signalling molecules like p38 and ERK1/2 were also reduced by two- and three-fold, respectively, after 30?min of treatment. Additionally, there was an increase in phosphorylated IκBα and down-regulation of p65 resulting in down-regulation of NF-κB pathway.

Conclusion Our results showed that 6G could modulate the anti-inflammatory responses triggered by V. cholerae-induced infection in intestinal epithelial cells by modulating NF-κB pathway.     

Hepatoprotective effect of Taraxacum officinale leaf extract on sodium dichromate‐induced liver injury in rats

Taraxacum officinale (L.) Weber, commonly known as Dandelion, has been widely used as a folkloric medicine for the treatment of liver and kidney disorders and some women diseases such as breast and uterus cancers. The main objective of the present study was to assess the efficiency of T. officinale leaf extract (TOE) in treating sodium dichromate hazards; it is a major environmental pollutant known for its wide toxic manifestations witch induced liver injury. TOE at a dose of 500 mg/kg b.w was orally administered once per day for 30 days consecutively, followed by 10 mg/kg b.w sodium dichromate was injected (intraperitoneal) for 10 days. Our results using Wistar rats showed that sodium dichromate significantly increased serum biochemical parameters. In the liver, it was found to induce an oxidative stress, evidenced from increase in lipid peroxidation and changes in antioxidative activities. In addition, histopathological observation revealed that sodium dichromate causes acute liver damage, necrosis of hepatocytes, as well as DNA fragmentation. Interestingly, animals that were pretreated with TOE, prior to sodium dichromate administration, showed a significant hepatoprotection, revealed by a significant reduction of sodium dichromate‐induced oxidative damage for all tested markers. These finding powerfully supports that TOE was effective in the protection against sodium dichromate‐induced hepatotoxicity and genotoxicity and, therefore, suggest a potential therapeutic use of this plant as an alternative medicine for patients with acute liver diseases. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 339–349, 2016.     

大黄、芒硝辅治急性重症胰腺炎33例效果观察及护理

目的:探讨对急性重症胰腺炎(SAP)患者在内科常规治疗的基础上行大黄胃管内注入和芒硝腹部外敷辅助治疗的效果和护理方法。方法:将66例患者随机分为观察组与对照组各33例,对照组行内科常规治疗,观察组在此基础上行大黄胃管内注入和芒硝腹部外敷治疗。观察两组患者治疗第5天时血淀粉酶下降幅度、治疗第10天时尿淀粉酶下降幅度、血、尿淀粉酶恢复正常的时间及治疗后腹痛和腹胀缓解、肠鸣音恢复、首次排便时间。结果:两组治疗第5天时血淀粉酶下降幅度、治疗第10天时尿淀粉酶下降幅度、血、尿淀粉酶恢复正常的时间比较差异均无统计学意义(P>0.05)。两组治疗后腹痛和腹胀缓解、肠鸣音恢复、首次排便时间比较差异有统计学意义(P<0.01)。结论:对SAP患者在常规治疗的基础上行大黄胃管内注入和芒硝腹部外敷辅助治疗可改善患者的症状,促进肠道功能恢复,缩短病程,促进康复。     

GC-MS法测定干姜超临界CO2萃取物的化学成分及其姜酚类成分的追踪

目的 分析干姜超临界CO2萃取物的化学成分,并追踪萃取物中的姜酚类成分.方法 采用超临界CO2萃取干姜药材,用气相色谱-质谱联用技术分析其成分,6-姜酚和1O-姜酚直接进样分析,将姜酚图谱与萃取物图谱进行对比分析.结果 从干姜超临界CO2萃取物中鉴定了52种成分.在6-姜酚和10-姜酚的气相色谱-质谱分析过程中追踪到两...     

铁皮石斛人工种子制作及影响因素研究

目的 建立铁皮石斛人工种子制作方法,并考察相关影响因素,为铁皮石斛的繁育提供一条新途径。方法 以铁皮石斛原球茎为包埋体制作人工种子,考察胚乳、种皮组分对人工种子萌发和成苗的影响。结果 以MS＋0.5 mg/L BA＋0.5 mg/L NAA＋3 g/L AC＋30 g/L海藻酸钠＋3 g/L百菌清为基本胚乳,在2% CaCl₂中反应15 min是铁皮石斛人工种子制作的较佳条件,胚乳中分别添加15 g/L木薯淀粉和10 g/L保水剂能明显提高人工种子的萌发率和成苗率,种皮中添加10 g/L纳米SiO₂和10 g/L纳米TiO₂均能明显提高萌发率,但添加10 g/L纳米SiO₂成苗率最高。结论 建立了铁皮石斛人工种子制作方法,获得了较高的萌发率和成苗率。     

基于代谢组学技术的大黄治疗慢性肾功能衰竭的作用机制研究

目的 利用代谢组学技术探讨大黄治疗慢性肾功能衰竭（CRF）的作用机制。方法 采用腺嘌呤制备大鼠CRF模型,以高分离度快速液相色谱-质谱（RRLC-MS）为核心分析技术,以主成分分析法为数据解析手段,筛选出CRF特征性内源代谢产物,探讨大黄治疗CRF的作用机制。结果 大黄能减弱或取消外界刺激因素（如腺嘌呤）诱发CRF,且对其代谢轨迹的扰动具明显的回调作用,其作用机制可能与潜在生物标志物有关。结论 大黄通过减少CRF大鼠血液中儿茶酚胺类物质生成、磷酸酯类物质分解、炎症介质产生,使体内D-谷氨酰胺、D-谷氨酸代谢和蛋氨酸循环恢复正常而发挥治疗CRF的作用。     

铁皮石斛多糖对RAW264.7细胞分泌TNF-α的影响

目的研究铁皮石斛多糖(polysaccharides from Den-drobium officinale,DOP)对小鼠巨噬细胞系RAW264.7细胞分泌TNF-α的影响并探讨其作用机制。方法 MTT法检测细胞活性;ELISA法检测TNF-α的分泌水平;反转录聚合酶链反应(RT-PCR)检测TNF-αmRNA表达量;Western blot技术检测胞质I-κBα蛋白的表达量。结果 DOP在20～160mg·L-1范围内明显促进RAW264.7细胞增殖,无细胞毒性;与空白对照组比较,DOP剂量依赖性地促进TNF-α的分泌;上调TNF-αmRNA表达;Western blot结果显示DOP能明显降低胞质内I-κBα蛋白水平。结论 DOP能增强RAW264.7细胞分泌TNF-α,其作用机制可能与降低胞质内I-κBα蛋白水平,活化核转录因子NF-κB,诱导TNF-αmRNA的表达有关。     

Noble dendrobium polysaccharides protects neuron against LPS-induced neurotoxicity in primary rat neuron/microglia culture

OBJECTIVE To investigate the protective effect of Noble dendrobium polysaccharides(NDP) on inflammatory factors,which are produced and released by 1ipopolysaecharide(LPS)-activated rat cerebral microglia,and to explore the protective mechanisms of NDP against LPS-induced neuron damage.METHODS The whole brains of 1 or 2-day-old mice was dissected,and microglia were isolated and cultured.Before exposure to LPS neurotoxicity,cells were treated with NDP(24 h),and the microglia-conditioned medium(MCM) collected.Primary neuronal cultures were supplemented with the 24 h MCM.The morphology and density of neuronal synapses were observed by immunofluorescence;the production of NO was detected with the Griess reagent;the level of tumor necrosis factor-α(TNF-α) was assessed by ELISA;the degree of neuronal apoptosis was examined with Hoechst 33258.RESULTS The hippocampal neurons were apparently damaged by the supernatant of activated MCM,and the morphology of the neurons changed significantly.Compared to control group,the level of NO was elevated and the expression level of TNF-α protein was significantly increased,and the apoptosis was induced in neurons.NDP improved synaptic morphology and increase synapses density,depress the high-level of NO,inhibited the up-expression of TNF-α protein by LPS,and decreased neuronal apoptosis.CONCLUSION NDP may significantly inhibit the activation of microglia induced by LPS and reduce the release of inflammatory factors.These results showed that NDP exert neuroprotection through depressing the actived microglia.