离乳大鼠假性性早熟模型的建立及对雌活性物质的应答

以雌激素含量明确的避孕药物作诱导剂观察了其对离乳Wistsar大鼠性成熟的影响,结果显示在给予避孕药后体重、乳腺、阴门、阴道上皮细胞、卵巢、子宫均发生类似人体假性性早熟变化,而肾上腺、脑垂体、甲状腺等与对照组比较均未见明显差异。     

cDNA cloning and mRNA expression of calponin and SM22 in rat aorta smooth muscle cells

We cloned and sequenced cDNAs encoding calponin (Calp) and SM22 (smooth muscle-specific 22-kDa protein) from rat aorta (RaA) smooth muscle (Smu) cells. The 1504-bp calp cDNA contains a single open reading frame (ORF) which encodes 297 amino acids (aa) (M_r 33 342). The 1186-bp SM22 cDNA contains a single ORF which encodes 201 aa (M_r 22 601). There were 43% identical aa in a 181-aa overlap between RaA Calp and SM22. Especially for the C-terminal region of SM22 and for the first repeat motif of Calp, 70% identity was observed. Northern blot analysis revealed that the calp and SM22 mRNAs were expressed in RaA Smu, but not in rat cardiac and skeletal muscles. SM22 mRNA was much more abundant than calp mRNA in RaA (3- to 4-fold). The expression levels of the calp and SM22 mRNAs in RaA showed a significant increase for 5 to 15 week old rats (1.5- to 3-fold) with vascular development and blood pressure elevation. No significant differences were observed in the expression of the RaA calp and SM22 mRNAs between normotensive (Wistar Kyoto) and spontaneously hypertensive rats (SHR).     

Ameliorative effects of nano Moringa on fluoride-induced testicular damage via down regulation of the StAR gene and altered steroid hormones

Fluoride is a common environmental contaminant that has harmful effects on human health when it is present in high concentrations. Fluoride enters the bloodstream after being absorbed by the gastrointestinal system when fluoride-contaminated groundwater is consumed by people. The aim of the present study was to determine whether polyphenol-rich nano Moringa oleifera (NMO) could protect rat testicles from sodium fluoride (NaF) damage by evaluating sperm quality, sex hormones, testicular oxidative status, histopathology, and StAR gene expression. Twenty-eight adult Wistar rats were divided equally and randomly into four groups: group one received distilled water; group two received NMO at a dosage of 250 mg/kg/body weight; group three received NaF at a dosage of 10 mg/kg/body weight; and group four received NaF and NMO. The rats were orally administrated daily for a duration of eight weeks. The study's findings demonstrated that, in comparison to rats exposed to NaF alone, co-administration of NMO and NaF enhanced sperm motility and viability, decreased sperm morphological changes, restored the balance between oxidant and antioxidant status, improved testosterone and dehydroepiandrosterone, improved testicular histology, raised the Johnson score, and upregulated the StAR gene in testicular tissue. These findings show that NMO is promise as a prophylactic medication against sodium fluoride-induced testicular damage because administration of NMO had no adverse effects and enhanced reproductive health.     

女贞子提取物对帕金森病大鼠神经炎性反应及内质网应激PERK/ATF4通路的影响

摘要 目的：探讨与分析女贞子提取物对帕金森病大鼠神经炎性反应及内质网应激蛋白激酶R样内质网激酶（PERK）/转录活化因子4（ATF4）通路的影响。方法：采用单侧注射6-羟基多巴胺（6-OHDA）毁损法建立帕金森病大鼠模型,将造模成功的大鼠36只随机平分为三组-模型组、左旋多巴组与女贞子组,每组各12只。左旋多巴组与女贞子组分别灌胃0.5 mL的左旋多巴、女贞子提取物,模型组给予无菌蒸馏水0.5 mL,2次/d,连续给药4周,检测大鼠神经炎性反应、内质网应激PERK/ATF4通路相关蛋白表达变化情况。结果：左旋多巴组与女贞子组治疗第2周、第4周的探究性反应次数显著高于模型组（P<0.05）,女贞子组与左旋多巴组对比也有显著提高（P<0.05）。左旋多巴组与女贞子组治疗第2周、第4周的脑组织伊文思蓝含量显著低于模型组（P<0.05）,女贞子组与左旋多巴组对比也有显著降低（P<0.05）。左旋多巴组与女贞子组治疗第2周、第4周的血清丙二醛、白介素-1β、肿瘤坏死因子-α、一氧化氮含量显著低于模型组（P<0.05）,女贞子组与左旋多巴组对比也有显著降低（P<0.05）。左旋多巴组与女贞子组治疗第2周、第4周的黑质-纹状体组织PERK蛋白、ATF4蛋白相对表达水平显著低于模型组（P<0.05）,女贞子组与左旋多巴组对比也有显著降低（P<0.05）。结论：女贞子提取物在帕金森病大鼠的应用能改善神经功能,降低脑组织伊文思蓝含量,还可抑制PERK/ATF4通路的激活,降低血清丙二醛、白介素-1β、肿瘤坏死因子-α、一氧化氮含量,从而持续发挥脑保护作用。     

Effect of dietary caffeine and zinc on the activity of antioxidant enzymes,zinc, and copper concentration of the heart and liver in fast-growing rats

The purpose of this study was to determine the relationship between concentrations of Zn and Cu and the activities of superoxide dismutase and glutathione peroxidase in the heart and liver of young rat pups whose dams were fed a diet supplemented with caffeine and/or Zn. Four groups of dams with their newborn pups were fed one of the following diets for 22 d: 20% protein basal diet; the basal diet supplemented with caffeine (2 mg/100 body wt); the basal diet supplemented with Zn (300 mg/kg diet); or the basal diet supplemented with caffeine plus Zn. The Cu levels in the livers of the pups were decreased by maternal intake of the caffeine and Zn diet. The maternal intake of the caffeine diet increased Mn-superoxide dismutase (MnSOD) activity and Cu, Zn-superoxide dismutase (CUZnSOD) in the heart of the pups. On the other hand, the activity of Cu,ZnSOD was significantly reduced in the liver of pups whose dams consumed a caffeine, Zn, or caffeine plus Zn diet. Cu, ZnSOD activity in the liver of the pups seems to be correlated with Cu levels in the tissue. Selenium-dependent glutathione peroxidase (GSH-Px) activities in the heart and liver showed no difference among the groups. The effect of dietary caffeine and/or Zn on the activity of antioxidant enzymes in the heart and liver were different in young rats. The activities of these enzymes in the heart were lower than in the liver of 22-d-old rats. Our experiments indicate that the heart has limited defenses against the toxic effects of peroxides when compared to the liver.     

Iodothyronine deiodinase activity in methionine-deficient rats fed selenium-deficient or selenium-sufficient diets

We examined the effect of methionine deficiency on iodothyronine 5’-deiodinase activity in selenium-deficient rats or selenium-sufficient rats fed sodium selenate or selenomethionine. Forty-two weanling male Wistar rats were divided into six groups and pair fed the respective purifiedl-amino acid-based diets for 4 wk.l-methionine concentrations in the diet were 8.0 g/kg for sufficient rats, and 2.0 g/kg for deficient rats. Selenium concentrations in the diet were 0.5 mg/kg (as sodium selenate or selenomethionine) for selenium-sufficient rats and less than 0.005 mg/kg for selenium-deficient rats. Type I 5’-deiodinase activities were significantly lower in liver and higher in kidney of methionine-deficient rats than in those of methionine-sufficient rats fed either the selenium-sufficient or the selenium-deficient diets. The type I 5’-deiodinase activity in brain was significantly lower in the methionine-deficient rats than in the methionine-sufficient rats fed the selenium-deficient diet. Type II 5’-deiodinase activity in brain was significantly higher in the methionine-deficient rats than in the methionine-sufficient rats fed selenium-sufficient diet as sodium selenate. Both thyroxine and 3,3’,5-triiodothyronine concentrations in plasma were significantly higher in the methionine-deficient rats than in the methionine-sufficient rats. It is suggested that the methionine deficiency affects the 5’-deiodinase activity and thyroid hormones level in the rats.     

Brain Quinolinic Acid in Chronic Experimental Hepatic Encephalopathy: Effects of an Exogenous Ammonium Acetate Challenge

Abstract: Elevated brain concentrations of the neurotoxin and NMDA receptor agonist quinolinic acid (QUIN) have been demonstrated in portacaval-shunted (PCS) rats, a chronic hepatic encephalopathy (HE) model. Increased brain QUIN levels have also been shown in acute hyperammonemic rats. In the present study, the plasma and brain (neocortical) QUIN levels in chronic PCS rats were investigated. The study also included a single exogenous ammonium acetate (NH₄Ac; 5.2 mmol/kg, i.p.) challenge to precipitate a reversible hepatic coma. Compared with sham-operated controls, chronic PCS rats exhibited decreased rather than increased plasma and brain QUIN levels. The plasma-to-brain QUIN ratio was not found to be altered. The NH₄Ac administration induced coma in all of the PCS rats 20–25 min after the challenge, and this coma was resolved within 60–75 min. No relevant temporal relationship between changes in brain QUIN levels and the neurological status in the PCS rats was observed. Therefore, our results do not support the contention that increased brain QUIN levels per se are involved in the pathogenesis of HE.     

Calcium concretions in the pineal gland of aged rats: an ultrastructural and microanalytical study of their biogenesis

The genesis of calcium concretions in aged rats was studied by means of transmission and scanning electron microscopy. The potassium pyroantimonate method, combined with X-ray microanalysis, allowed us to study the distribution of cations and calcium. Notable accumulations of calcium (associated with phosphorus) were localized in vesicles, vacuoles, lipid droplets, lipopigments, and mitochondria of dark pinealocytes. The results obtained in the present investigation suggest that these organelles are involved in the genesis of the concretions. The presence of sulfur indicates the existence of an organic matrix. We propose that genesis takes place in dark pinealocytes, which contain more calcium than light pinealocytes. Mineralization foci are some-times associated with cellular debris and enlarge by further apposition of material. Two types of concretions, as determined by electron microscopy and confirmed by electron diffraction, could be observed: the amorphous type with concentric layers and the crystalline type with needle-shaped crystals. Once formed, the concretions reach the extracellular space and the cell breaks down. Possible extracellular calcification is suggested in the extracellular calcium-rich floculent material. The mineralization process is interpreted as being an age-related phenomenon and mainly a consequence of the degeneration of pinealocytes.     

Ultrastructural localization of nitric oxide synthase and endothelin in coronary and pulmonary arteries of newborn rats

This is the first report on the ultrastructural distribution of nitric oxide synthase and endothelin immunoreactivities in the coronary and pulmonary arteries of newborn Wistar rats. The distribution of nitric oxide synthase and endothelin was investigated using pre-embedding peroxidase-antiperoxidase immunocytochemistry. In both arteries examined, positive labelling for nitric oxide synthase was localized both in the endothelium and smooth muscle, whereas positive labelling for endothelin was localized in the endothelium exclusively. In the coronary artery, approximately 80% and 55% of the endothelial cells examined were positive for nitric oxide synthase and endothelin, respectively, whereas in the pulmonary artery, 77% and 60% of the endothelial cells were positive for nitric oxide synthase and endothelin, respectively. These findings indicate that nitric oxide synthase and endothelin are colocalized in some of the endothelial cells of the newborn rat. In the endothelium, nitric oxide synthase and endothelin immunoreactivities were distributed throughout the cell cytoplasm and in association with the membranes of intracellular organelles. In smooth muscle, a relationship of nitric oxide synthase immunoreactivity to endoplasmic reticulum was observed in the pulmonary artery. In summary, in the newborn rat, endothelial cells of the coronary and pulmonary artery are rich in nitric oxide synthase (neuronal isoform) and endothelin, and it is suggested therefore that they may be substantially involved in vasomotor control of the cardiac and pulmonary circulation during early stages of postnatal development.