Gastric emptying of hexose sugars: role of osmolality,molecular structure and the CCK1 receptor

Background It is widely reported that hexose sugars slow gastric emptying (GE) via osmoreceptor stimulation but this remains uncertain. We evaluated the effects of a panel of hexoses of differing molecular structure, assessing the effects of osmolality, intra‐individual reproducibility and the role of the CCK₁ receptor, in the regulation of GE by hexoses. Methods Thirty one healthy non‐obese male and female subjects were studied in a series of protocols, using a ¹³C‐acetate breath test to evaluate GE of varying concentrations of glucose, galactose, fructose and tagatose, with water, NaCl and lactulose as controls. GE was further evaluated following the administration of a CCK₁ receptor antagonist. Three subjects underwent repeated studies to evaluate intra‐individual reproducibility. Key Results At 250 mOsmol, a hexose‐specific effect was apparent: tagatose slowed GE more potently than water, glucose and fructose (P < 0.05). Fructose (P < 0.05) also slowed GE, but with substantial inter‐, but not intra‐, individual differences. As osmolality increased further the hexose‐specific differences were lost. At 500 mOsmol, all hexoses slowed GE compared with water (P < 0.05), whereas lactulose and saline did not. The slowing of GE by hexose sugars appeared to be CCK₁ receptor‐dependent. Conclusions & Inferences The effects of hexose sugars on GE appear related to their molecular structure rather than osmolality per se, and are, at least in part, CCK₁ receptor‐dependent.     

Haemaphysalis longicornis tick bites are a possible cause of red meat allergy in Japan

Recent studies revealed that Amblyomma or Ixodes tick bites may cause red meat allergy, in which galactose‐α‐1,3‐galactose (α‐Gal) is a major IgE‐binding epitope. The incidence of red meat allergy is high in Shimane Prefecture, as is tick‐transmitted Japanese spotted fever. Therefore, we speculated that tick bites may cause these meat allergies. The carbohydrate α‐Gal was detected in the salivary gland protein of Haemaphysalis longicornis (H. longicornis), the vector for Japanese spotted fever, by immunoblotting using anti‐α‐Gal antibody. H. longicornis salivary gland protein‐specific IgE was detected in the sera of 24 of 30 patients with red meat allergies. Sensitization to tick salivary gland protein containing α‐Gal is possibly a major etiology of red meat allergy; the carbohydrate plays a crucial role in its allergenicity. These results further indicate that the α‐Gal epitope is present not only in Amblyomma or Ixodes, but also in Haemaphysalis.     

水蛭滴眼液防治半乳糖白内障的实验研究

目的 探讨水蛭滴眼液对半乳糖白内障的防治作用。方法 用SD大鼠复制半乳糖白内障模型,以水蛭为主要成分,配制成水蛭滴眼液,并以白内停滴眼液为阳性对照药,动态观察并比较两组滴眼液对半乳糖白内障的影响。于实验第10天测定两组晶状体的超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px),谷胱甘肽(GSH)和可溶性蛋白(SP)的含量。结果 水蛭组较对照组晶状体混浊速度慢,程度也轻。水蛭组SOD,GSH-Px,GSH的含量均显著高于对照组。结论水蛭滴眼液具有较好的延缓和减轻半乳糖白内障的作用,且优于白内停滴眼液。     

急性致衰老动物模型的探讨

为探讨一种快速简便的衰老动物模型 ,采用γ射线辐射SD大鼠后 ,测定其超氧化物歧化酶 (SOD)与丙二醛 (MDA)的变化及给小鼠颈背部皮下连续注射D 半乳糖后 ,测定其SOD与MDA的变化。结果表明(1)γ 射线辐照法 :SOD活力 (nU ml)实验组为 15 3± 46 ,对照组为 2 0 2± 6 0 ;MDA的含量 (nmol ml)实验组为 2 70± 75 ,对照组为 2 5 3 2± 2 0 8。辐照后两组的SOD活力和MDA含量有显著性差异 ,且SOD活力显著下降 ,MDA含量显著升高。 (2 )D 半乳糖法 :其结果与辐照法相同。提示在短期内用γ射线辐照的SD大鼠 ,能做为衰老动物模型     

关龙胆提取物的保护肝脏作用实验研究

[目的 ]探讨关龙胆提取物对肝脏的保护作用 .[方法 ]采用D 氨基半乳糖和内毒素制作小鼠急性肝损伤模型 ,观察关龙胆水提取物和乙醇提取物对急性肝损伤小鼠的血清丙氨酸转氨酶及天冬氨酸转氨酶活性的影响 ,并且观察小鼠肝组织的病理改变 .[结果 ]腹腔注射 10 0mg/kg关龙胆乙醇提取物可明显降低因D 氨基半乳糖及内毒素所致急性肝损伤小鼠的血清丙氨酸转氨酶及天冬氨酸转氨酶的活性 ,与模型组比较有显著性差异 .[结论 ]关龙胆乙醇提取物对D 氨基半乳糖及内毒素所致小鼠急性肝损伤有保护作用     

Laser Raman Spectrometry Study on Experimental Galactose-induced Cataract

Purpose: To observe the dynamic changes of hydration in galactose induced cataract.Methods: Two groups of wistar rats were used in the experiment. There were 12 rats in the experimental group, which were fed diet of 50% D-Galactose standard feed ; while the control group had 8 rats fed standard feed. Their other living conditions were the same. At desired time periods, two Wistar rats fed galactose and one normal control were selected and killed 20 minutes before the instrument examination respectively, them, their lenses were removed from the orbs by a posterior approach. The cleaned fresh lens was placed in a quartz cuvette with Tris buffered balanced salt solution containing 5. 5 mmol/L glucose. The quartz cuvette was placed on the stage of the Spectrometer. The laser beam was focused at the lens nuclear from the bottom of the cuvette and the scattered light was collected at 90?to the incident beam.Results: Raman spectroscopy showed that (1) during the formation of galactose cataract, the water signa     

D‐galactose‐induced toxicity associated senescence mitigated by alpinate oxyphyllae fructus fortified adipose‐derived mesenchymal stem cells

This study addresses the effect of D‐galactose‐induced toxicity associated senescence mitigated by alpinate oxyphyllae fructus (AOF; Alpinia oxyphylla Miq) extracts fortified with adipose‐derived mesenchymal stem cells (ADMSCs) in rats. Male 18 week‐old Wistar Kyoto (WKY) rats were used in this study. We analyzed cardiac fibrosis by Masson's trichrome staining. The tissue sections were dyed using hematoxylin and eosin (H&E). Tissue sections were stained for the restoration of Nrf2 expression in treatment groups by immunohistochemistry. Immunohistochemistry and western blotting analysis showed that AOF with ADMSCs could significantly reduce aging‐induced oxidative stress in D‐galactose‐induced aging rat hearts by inducing Nrf2 pathway. Reduction in ROS resulted in the suppression of inflammatory signals (p‐NF‐κB and IL‐6). Histopathological studies were showed an increased interstitium and collagen accumulation in aging‐induced heart sections. However, AOF and ADMSCs treated hearts were recovered from cardiac remodeling. Furthermore, hypertrophy and fibrosis associated markers were also significantly reduced (P < .05) in treatment groups. We speculate that ADMSCs might activate certain paracrine factors, which could target the upstream activator of aging associated cardiac complications and AOF might provide homing for these stem cells.     

半乳糖受体介导的c-myc反义核酸对人肝癌细胞

目的 :探讨半乳糖 (Gal) -聚乙烯亚胺 (PEI) -c -myc反义寡核苷酸 (ASODN)交联复合物对人肝癌细胞增殖的影响。方法 :Gal-PEI-ASODN复合物作用于人肝癌Bel- 74 0 2细胞 ,台盼蓝染色法检测不同时间、不同浓度作用下细胞增殖的变化 ,倒置显微镜观察细胞形态 ,流式细胞仪分析细胞亚二倍体的百分率 ,透射电镜观察细胞超微结构的改变。结果 :在 0 - 96h的不同时间点 ,与ASODN组 (含ASODN 2 0 μmol/L)相比 ,Gal-PEI-ASODN复合物 (含ASODN 0 75 μmol/L)明显抑制Bel- 74 0 2细胞的增殖 ,Gal-PEI -ASODN复合物的起效浓度更低 ,起效时间更短 ;不同浓度的单纯ASODN与Bel- 74 0 2细胞作用 72h ,测得ASODN的IC50 为 2 0 9μmol/L ,而在半乳糖受体的介导下 ,ASODN与Bel- 74 0 2细胞作用 4 8h ,测得ASODN的IC50 为 0 2 94 μmol/L ,ASODN的抑制效果提高 70 9倍 ;Gal-PEI -ASODN复合物与Bel- 74 0 2细胞作用 4 8h ,与单纯ASODN组相比 ,细胞亚二倍体百分率更高 ,并且电镜下可见明显的细胞凋亡形态。结论 :半乳糖受体介导的投递系统可明显提高ASODN对Bel- 74 0 2细胞的增殖抑制效应     

Binding of glycophorins to Plasmodium falciparum merozoites

Plasmodium falciparum merozoites recognize and attach to glycophorins, the surface sialoglycoproteins of human erythrocytes. The structural requirements for a merozoite binding site were studied with the use of two methods. In the first, certain glycophorins and their tryptic fragments were added directly to isolated merozoites prior to their addition to erythrocytes. Low concentrations (50 micrograms ml-1) of glycophorin A inhibited merozoite invasion. At higher concentrations a mixture of glycophorins A, B and C (GPS) (100 micrograms ml-1) and glycophorin B (200 micrograms ml-1) also inhibited invasion. GPS from Tn erythrocytes which lack both sialic acid and galactose residues was almost as effective as normal GPS in blocking invasion. None of the monosaccharides present on glycophorin, including N-acetylneuraminic acid, inhibited merozoite invasion. Erythrocytes treated with lectins were only partially resistant to invasion. These results indicated that the oligosaccharide side chains are not the major structural determinant of the merozoite binding site. Glycophorin A was cleaved by trypsin and the separated fragments added to merozoites. Only the external N-terminal tryptic fragment T1 and the trypsin resistant hydrophobic core, T6, showed some, but considerably less, inhibitory activity than the intact molecule. In the second approach, the binding of 125I-labeled GPS to isolated merozoites was determined. 125I-GPS binding was saturated at 0.23 micrograms for 10(9) merozoites and was competitively inhibited by unlabeled GPS but not by free sugars. Desialylated GPS bound almost to the same extent as the intact molecule.