ANTIUROLITHIC ACTIVITY OF AQUEOUS EXTRACT OF ROOTS OF CISSAMPELOS PAREIRA IN ALBINO RATS

                                                        ABSTRACT Objective:      To evaluate the antiurolithic activity of aqueous extract of roots of Cissampelos pareira (AQERCP) in 2% Ammonium chloride (AC) and 0.75% Ethylene glycol (EG) induced urolithiasis in albino rats. Methods :  Urolithiasis was induced in rats by supplying drinking water mixed with 2 % (AC) and 0.75 % (EG) for 10 days. Calculi were confirmed by the high urinary levels of calcium, uric acid and low levels of magnesium and high levels of serum creatinine and calcium. The animals were treated with 03 doses of AQERCP i.e., 100 mg/kg, 200 mg/kg, 400 mg/kg respectively orally in different groups of rats once daily for 10 days along with 2 % (AC) and 0.75% (EG) mixed drinking water. On 11th day 3 rats from each group were kept in one metabolic cage and urine (pooled) collected for 24 h was subjected for estimation of various biochemical parameters. Blood was collected on the same day and analysed for various parameters. Kidneys were observed for the histopathological changes.Results: Rats treated with 03 doses of AQERCP significantly (P≤ 0.05) reduced urinary calcium, uric acid and increased urinary magnesium levels, reduced serum calcium, creatinine and increased serum magnesium. Histopathology of kidneys in groups treated with AQERCP at 200 mg/kg and 400 mg/kg doses revealed less tissue damage and the cytology of nephrotic tissue was almost similar to the control Group I rats.Conclusion :              Results showed AQERCP has shown significant antiurolithic effect against chemical induced urolithiasis in rats.Keywords :  C.pareira,  Roots extracts, Antiurolithic activity, Ammonium chloride, Ethylene glycol .                                                     Â

Discovery of an α2,9-PolyNeu5Ac Glycoprotein in C-1300 Murine Neuroblastoma (Clone NB41A3)

alpha2,8-PolyNeu5Ac is expressed on neural cell adhesion molecules during embryogenesis and also re-expressed on certain tumors. PolyNeu5Ac is therefore an oncodevelopmental antigen, has important regulatory effects on the adhesive and migratory behavior of neural cells, and is thus crucial to synaptic plasticity. Until now, alpha2,9-polyNeu5Ac, a linkage isomer of alpha2,8-polyNeu5Ac, has long been thought to occur only in capsules of neuroinvasive Neisseria meningitidis group C bacteria. Here we report the unexpected discovery of alpha2,9-polyNeu5Ac in a new cell adhesion-related glycoprotein on the membrane of C-1300 murine neuroblastoma cells (clone NB41A3). We also report the expression of alpha2,9-polyNeu5Ac was affected by cell growth and retinoic acid-induced differentiation. Occurrence of the linkage isomer of alpha2,8-polyNeu5Ac has been left unrecognized by conventional methods using biological diagnostic probes for alpha2,8-polyNeu5Ac. Thus, our discovery may change contemporary views of biology and pathology of polysialic acid and open new avenues for the development of anti-neural tumor drugs

Diuretic activity of aqueous extract of roots of Cissampelos pareira in albino rats

Background: Diuretic compounds that stimulate the excretion of water with small traceable ions are potentially useful in most of disorders including those exhibiting edema such as congestive heart failure, nephritis, toxemia of pregnancy, premenstrual tension, and hypertension. The aim was to evaluate the diuretic activity of aqueous extract of roots of Cissampelos pareira (AQERCP) by Lipschitz method in albino rats.Methods: Five groups of Albino rats were used to evaluate the diuretic activity of AQERCP by using metabolic cages. The Group I serves as normal control received vehicle (carboxymethyl cellulose 2% in normal saline), the Group II furosemide (10 mg/Kg, p.o) in vehicle; other Groups III, IV, and V were treated with low (100 mg/kg), medium (200 mg/kg), and high (400 mg/kg) doses of AQERCP in vehicle. Immediately, after the extract treatment all the rats were hydrated with saline (15 ml/kg, p.o) and placed in the metabolic cages (3/cage), specially designed to separate urine and faeces, kept at 21°C±0.5°C.The total volume of urine collected was measured at the end of 5th hr. During this period, no food and water was made available to animals. Various parameters such as total urine volume and concentration of sodium, potassium, chloride ions in the urine were measured and estimated respectively.Results: In this model, when compared to vehicle treated control group the AQERCP at different dose levels (100, 200 and 400 mg/kg) has significantly increased the urine volume and also enhanced the elimination of sodium, potassium and chloride ions in urine.Conclusion: The results showed that single dose administration of AQERCP as 100, 200 and 400 mg/Kg and standard frusemide (10 mg/kg b.wt) has significantly (p<0.05*, p<0.01**, p<0.001***) increased the urine output along with an increase in concentration of sodium, potassium, and chloride. AQERCP 400 mg/Kg produced a greater diuretic activity, which is comparable to the effect of standard furosemide (10 mg/kg).The present study has supported and justified the basis for folklore use of roots of C. pareira as a diuretic agent

Ectodermal Wnt6 is an early negative regulator of limb chondrogenesis in the chicken embryo

Background: Pattern formation of the limb skeleton is regulated by a complex interplay of signaling centers located in the ectodermal sheath and mesenchymal core of the limb anlagen, which results, in the forelimb, in the coordinate array of humerus, radius, ulna, carpals, metacarpals and digits. Much less understood is why skeletal elements form only in the central mesenchyme of the limb, whereas muscle anlagen develop in the peripheral mesenchyme ensheathing the chondrogenic center. Classical studies have suggested a role of the limb ectoderm as a negative regulator of limb chondrogenesis. Results: In this paper, we investigated the molecular nature of the inhibitory influence of the ectoderm on limb chondrogenesis in the avian embryo in vivo. We show that ectoderm ablation in the early limb bud leads to increased and ectopic expression of early chondrogenic marker genes like Sox9 and Collagen II, indicating that the limb ectoderm inhibits limb chondrogenesis at an early stage of the chondrogenic cascade. To investigate the molecular nature of the inhibitory influence of the ectoderm, we ectopically expressed Wnt6, which is presently the only known Wnt expressed throughout the avian limb ectoderm, and found that Wnt6 overexpression leads to reduced expression of the early chondrogenic marker genes Sox9 and Collagen II. Conclusion: Our results suggest that the inhibitory influence of the ectoderm on limb chondrogenesis acts on an early stage of chondrogenesis upsteam of Sox9 and Collagen II. We identify Wnt6 as a candidate mediator of ectodermal chondrogenic inhibition in vivo. We propose a model of Wnt-mediated centripetal patterning of the limb by the surface ectoderm.Dentistry, Faculty ofOral Health Sciences (OHS), Department ofNon UBCReviewedFacult

FGFs, Wnts and BMPs mediate induction of VEGFR-2 (Quek-1) expression during avian somite development

AbstractRegulation of VEGFR-2 (Quek1) is an important mechanism during blood vessel formation. In the paraxial mesoderm, Quek1 expression is restricted to the lateral portion of the somite and later to sclerotomal cells surrounding the neural tube. By implanting FGF 8b/8c or SU 5402 beads into the paraxial mesoderm, we show that FGF8 in addition to BMP4 from the intermediate mesoderm (IM) is a positive regulator of VEGFR-2 (Quek1) expression in the quail embryo. The expression of Quek1 in the medial somite half is normally repressed by the notochord and Sfrps-expression in the neural tube. Over-expression of Wnt 1/3a also results in an up-regulation of Quek1 expression in the somites. We also show that up-regulation of FGF8/Wnt 1/3a leads to an increase in the number of endothelial cells, whereas inhibition of FGF and Wnt signaling by SU 5402 and Sfrp-2 results in a loss of endothelial cells. Our results demonstrate that the regulation of Quek1 expression in the somites is mediated by the cooperative actions of BMP4, FGF8 and Wnt-signaling pathways