Brain scarring in infants:immunological insights from a neonatal hypoxic-ischemic encephalopathy model

Neonatal hypoxic-ischemic encephalopathy(HIE)is a significant cause of disability in children.Improving brain function and accelerating neurological recovery may require a combination of neuroprotective and pro-regenerative treatments at different stages of HIE.While the first hours after the neonatal insult are the most critical period for neuroprotection,the existence of secondary and tertiary mechanisms of brain injury offers the possibility of preventing delayed neurodegeneration in the subsequent days,weeks,or months(Levison et al.,2022).

The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury

We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury.

Does MgSO_(4) protect the preterm brain?Dissecting its role in the pathophysiology of hypoxic ischemic encephalopathy

Mitigating preterm encephalopathy continues to be one of the greatest challenges in perinatal medicine.Preterm encephalopathy is associated with high mortality,serious morbidity,and significant socio-economic impacts on the individuals,their families,and public health sectors and welfare systems that last a lifetime.The cost of disability associated with preterm brain injury continues to rise.Prevention of this injury,and disability,would significantly reduce this socioeconomic burden.

Sodium Sulfite as a Novel Hypoxia Revulsant Involved in Hypoxic Regulation in Escherichia coli

As a reducing salt,sodium sulfite could deprive oxygen in solution,which could mimic hypoxic stress in Caenorhabditis elegans.In this study,the wildtype Escherichia coli strain MG1655 was used to examine the inhibition of sodium sulfite-induced hypoxia by observing the bacterial growth curves.

Dunbar Syndrome and Hypoxic Hepatitis: An Unusual Presentation

Hypoxic hepatitis, also known as ischemic hepatitis, is characterized by acute hepatocellular injury due to inadequate oxygen delivery to the liver. Celiac trunk stenosis can lead to hepatic ischemia and subsequent liver damage. We present the case of an 81-year-old patient with a history of hypertension, ischemic heart disease, hypothyroidism, and biliary lithiasis, who developed hypoxic hepatitis secondary to Dunbar syndrome and a stenosis of the superior mesenteric artery. The patient improved symptoms and liver function tests with conservative management, including intravenous fluids and supportive care. Long-term management involved continued antiplatelet therapy and statins, with consideration of further interventions for celiac trunk stenosis. This case underscores the importance of recognizing Dunbar syndrome as well as superior mesentery trunk stenosis as a potential cause of hypoxic hepatitis. It highlights the need for multidisciplinary management in such cases.

Spectrum of delayed post-hypoxic leukoencephalopathy syndrome:A systematic review

BACKGROUND Delayed post hypoxic leukoencephalopathy syndrome(DPHLS),also known as Grinker’s myelinopathy,is a rare but significant neurological condition that manifests days to weeks after a hypoxic event.Characterized by delayed onset of neurological and cognitive deficits,DPHLS presents substantial diagnostic and therapeutic challenges.AIM To consolidate current knowledge on pathophysiology,clinical features,diagnostic approaches,and management strategies for DPHLS,providing a comprehensive overview and highlighting gaps for future research.METHODS Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes guidelines,we systematically searched PubMed,ScienceDirect and Hinari databases using terms related to delayed post-hypoxic leukoencephalopathy.Inclusion criteria were original research articles,case reports,and case series involving human subjects with detailed clinical,neuroimaging,or pathological data on DPHLS.Data were extracted on study characteristics,participant demographics,clinical features,neuroimaging findings,pathological findings,treatment,and outcomes.The quality assessment was performed using the Joanna Briggs Institute critical appraisal checklist.RESULTS A total of 73 cases were reviewed.Common comorbidities included schizoaffective disorder,bipolar disorder,hypertension,and substance use disorder.The primary causes of hypoxia were benzodiazepine overdose,opioid overdose,polysubstance overdose,and carbon monoxide(CO)poisoning.Symptoms frequently include decreased level of consciousness,psychomotor agitation,cognitive decline,parkinsonism,and encephalopathy.Neuroimaging commonly revealed diffuse T2 hyperintensities in cerebral white matter,sometimes involving the basal ganglia and the globus pallidus.Magnetic resonance spectroscopy often showed decreased N-acetylaspartate,elevated choline,choline-to-creatinine ratio,and normal or elevated lactate.Treatment is often supportive,including amantadine,an antioxidant cocktail,and steroids.Hyperbaric oxygen therapy may be beneficial in those with CO poisoning.Parkinsonism was often treated with levodopa.Most of the patients had substantial recovery over the course of months and many cases had some residual neurocognitive deficits.CONCLUSION DPHLS remains a complex and multifaceted condition with various etiologies and clinical manifestations.Early recognition and appropriate management are crucial to improving patient outcomes.Future research should focus on standardizing diagnostic criteria,using advanced imaging techniques,and exploring therapeutic interventions to improve understanding and treatment of DPHLS.Conducting prospective cohort studies and developing biomarkers for early diagnosis and monitoring will be essential to advance patient care.

Intestinal glucagon-like peptide-1 in hypoglycemic counterregulation for type 1 diabetes management

Type 1 diabetes(T1D)is characterized by the autoimmune destruction of pan-creatic beta cells,leading to absolute insulin deficiency and the need for exoge-nous insulin.A significant concern in T1D management is hypoglycemia,which is worsened by impaired counterregulatory mechanisms.Effective counterregu-lation involves hormones such as glucagon and adrenaline,which work to restore normal blood glucose levels.However,in T1D,these mechanisms often fail,par-ticularly after recurrent hypoglycemia,resulting in hypoglycemia-associated au-tonomic failure.Recent research indicates that elevated levels of intestinal glu-cagon-like peptide-1(GLP-1)impair counterregulatory responses by reducing the secretion of glucagon and adrenaline.This editorial underscores GLP-1’s role be-yond its incretin effects,contributing to impaired hypoglycemic counterregu-lation.This understanding necessitates a nuanced approach to GLP-1-based the-rapies in T1D,balancing the benefits of glycemic control with potential risks.Future research should delve into the mechanisms behind GLP-1’s effects and explore potential interventions to improve hypoglycemic counterregulation.The goal is to enhance the safety and quality of life for T1D patients.

miRNA-21-5p is an important contributor to the promotion of injured peripheral nerve regeneration using hypoxia-pretreated bone marrow-derived neural crest cells

Our previous study found that rat bone marrow–derived neural crest cells(acting as Schwann cell progenitors)have the potential to promote long-distance nerve repair.Cell-based therapy can enhance peripheral nerve repair and regeneration through paracrine bioactive factors and intercellular communication.Nevertheless,the complex contributions of various types of soluble cytokines and extracellular vesicle cargos to the secretome remain unclear.To investigate the role of the secretome and extracellular vesicles in repairing damaged peripheral nerves,we collected conditioned culture medium from hypoxia-pretreated neural crest cells,and found that it significantly promoted the repair of sensory neurons damaged by oxygen-glucose deprivation.The mRNA expression of trophic factors was highly expressed in hypoxia-pretreated neural crest cells.We performed RNA sequencing and bioinformatics analysis and found that miR-21-5p was enriched in hypoxia-pretreated extracellular vesicles of neural crest cells.Subsequently,to further clarify the role of hypoxia-pretreated neural crest cell extracellular vesicles rich in miR-21-5p in axonal growth and regeneration of sensory neurons,we used a microfluidic axonal dissociation model of sensory neurons in vitro,and found that hypoxia-pretreated neural crest cell extracellular vesicles promoted axonal growth and regeneration of sensory neurons,which was greatly dependent on loaded miR-21-5p.Finally,we constructed a miR-21-5p-loaded neural conduit to repair the sciatic nerve defect in rats and found that the motor and sensory functions of injured rat hind limb,as well as muscle tissue morphology of the hind limbs,were obviously restored.These findings suggest that hypoxia-pretreated neural crest extracellular vesicles are natural nanoparticles rich in miRNA-21-5p.miRNA-21-5p is one of the main contributors to promoting nerve regeneration by the neural crest cell secretome.This helps to explain the mechanism of action of the secretome and extracellular vesicles of neural crest cells in repairing damaged peripheral nerves,and also promotes the application of miR-21-5p in tissue engineering regeneration medicine.

Antioxidant and Hypoglycemic Ability of Ardisia gigantifolia Stapf Parts

[Objectives]To study the antioxidant and hypoglycemic effects of different parts of Ardisia gigantifolia Stapf.[Methods]The hydroxyl radical scavenging activity,DPPH radical scavenging activity and total antioxidant capacity of ABTS of 75%ethanol extract of A.gigantifolia Stapf and the petroleum ether,ethyl acetate,n-butanol,chloroform and aqueous extract were measured with Vc as positive control.At the same time,acarbose was used as reference substance to determine the inhibitory effect of each polar site onα-glucosidase.[Results]All parts of A.gigantifolia Stapf had antioxidant activity,among which ethyl acetate had the strongest antioxidant activity,and the scavenging rate of hydroxyl radical and DPPH radical was higher than that of positive control.The results showed that petroleum ether,ethyl acetate and chloroform had a good inhibitory effect onα-glucosidase(better than acarbose).[Conclusions]The ethyl acetate part of A.gigantifolia Stapf had the best antioxidant activity and inhibitory effect onα-glucosidase.It provides a basis for further research and development of A.gigantifolia Stapf.

Analysis of the Effect of Outpatient Nursing Intervention on Hypoglycemic Treatment Effect and Psychological Emotions of Diabetic Patients

Objective:To explore the effect of outpatient nursing interventions on the hypoglycemic treatment and psychological emotions of diabetic patients.Methods:148 patients who came to our hospital for outpatient treatment from February 2022 to October 2023 were selected and divided into a control group and an observation group,with 74 cases per group,according to the random number table method.The control group received routine nursing intervention,and the observation group received outpatient nursing intervention based on the control group.The two groups were observed for their effects of hypoglycemic treatment and psychological and emotional improvement before and after outpatient nursing intervention.Results:The health behavior scores of the control group were lower than that of the observation group;the post-intervention fasting blood glucose,2h postprandial blood glucose,anxiety self-rating scale(SAS),and the depression self-rating scale(SDS)of the control group were significantly higher than that of the observation group,and the difference was statistically significant(P<0.01).Conclusion:Outpatient nursing intervention encouraged patients to comply with healthy behaviors and helped control blood sugar levels.Patients’anxiety,depression,and other adverse psychological states were also improved hence the outpatient nursing intervention is worthy of further promotion.

Hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect neurons from cardiac arrest-induced pyroptosis

Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to improve migration and survival of bone marrow–derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest,but the specific mechanisms by which hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown.To this end,we established an in vitro co-culture model of bone marrow–derived mesenchymal stem cells and oxygen–glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis,possibly through inhibition of the MAPK and nuclear factor κB pathways.Subsequently,we transplanted hypoxia-preconditioned bone marrow–derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia.The results showed that hypoxia-preconditioned bone marrow–derived mesenchymal stem cells significantly reduced cardiac arrest–induced neuronal pyroptosis,oxidative stress,and mitochondrial damage,whereas knockdown of the liver isoform of phosphofructokinase in bone marrow–derived mesenchymal stem cells inhibited these effects.To conclude,hypoxia-preconditioned bone marrow–derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest,and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.

Antioxidant Activity of Polysaccharides in Yam Bulbils and Their Hypoglycemic Effect in Diabetic Mice

The polysaccharides in yam bulbils were extracted, and their antioxidant activity and hypoglycemic effect in diabetic mice were discussed. The results showed that the antioxidant activity of polysaccharides in yam bulbils was signifi- cantly enhanced with the increase of concentration; they showed a strong scaveng- ing ability against DPPH. and .OH, and the scavenging ability was dose dependent to some extent; the scavenging rates reached 91.15% and 89.06% respectively when the dose reached 4.0 mg/ml; the polysaccharides in yam bulbils significantly educed the blood glucose in model rice, and the hypoglycemic effect of large-dose polysaccharides was more obvious. The polysaccharides in yam bulbils has good antioxidant activity and hypoglycemic effect, which provides a new source for devel- opment of safe and natural food antioxidants and blood sugar-lowering agents.

Effect of Chitosan-Cysteine Conjugate on Enzymatic Degradation and Hypoglycemic effect of Insulin

Aim To evaluate the inhibitory effect of chitosan-cysteine conjugate onenzymatic degradation and hypogly-cemic enhancement effect of insulin. Methods Chitosan-cysteineconjugate was synthesized. The protective effect of the conjugate against degradation of insulin byα-chymotrypsin and trypsin was evaluated in vitro. Insulin enteric- microspheres were prepared byusing O_1 /Q_2 emulsion solvent evaporation method. The hypoglycemic enhancement effect of theconjugate was studied by oral administration of insulin solution or enteric-microspheres to rats.Results The thiol group content of the synthesized conjugate was about 200 μmol·g^(-1) polymer,which showed a strong protective effect on insulin from enzymatic degradation in vitro. Almost allthe insulin incubated in a-chymotrypsin solution or trypsin solution without chitosan-cysteineconjugate was degraded entirely within 1 h and 5 h respectively, whereas above 75% of insulinremained in the same content of the enzymatic solution containing 4 mg·mL^(-1) conjugate. The drugloading of insulin enteric-microspheres was about 7% . In vivo experiment, chitosan-cysteineconjugate (85 μg·kg^(-1)) prolonged the hypoglycemic time of insulin solution orenteric-microspheres when administered simultaneously with the absorption enhancer SNAC. ConclusionChitosan-cysteine conjugate has a marked inhibitory effect on the enzymatic degradation of insulinin vitro, and it displays a significant hypoglycemic enhancement effect on insulin oral formulationin vivo.

A Comparative Analysis of the Administration of Oral Hypoglycemic Drugs in Second Affiliated Hospital of Guiyang Medical College during 2012-2014

[Objective] This study aimed to analyze the application and administration of oral hypoglycemic drugs in Second Affiliated Hospital of Guiyang Medical College,aiming at providing guidance and reference for clinical medication for treatment of diabetes.[Method] The main types,dosages and prices of oral hypoglycemic drugs in Second Affiliated Hospital of Guiyang Medical College during 2012-2014 were compared and analyzed using the computer network system.[Result] During 2012-2014,sales quantity and sales amount of oral hypoglycemic drugs in Second Affiliated Hospital of Guiyang Medical College demonstrated an upward trend.[Conclusion] Integrative medicine can significantly improve symptoms of diabetes complications.Certain achievements have been made in diabetes treatment by Second Affiliated Hospital of Guiyang Medical College.

Hypoglycemic effect of Brassica juncea(seeds) on streptozotocin induced diabetic male albino rat

Objective:To evaluate the hypoglycemic effect of Brassica juncea(seeds) on streptozotocin induced diabetic male albino rats.Methods:Hypoglycemic activity of Brassica juncea(seeds)aqueous extract at a dose of 250,350 and 450 mg/kg body weight was evaluated.Adult male Swiss albino rats of six numbers in each group was undertaken for study and evaluated.Results:The serum insulin levels were recorded a significant depletion in all groups,short term as well as long term diabetic animals,when compared to that of normal animals.A significant dosage dependent augmenting effect of the seed extract on the serum insulin was recorded in both short term as well as long term groups.Conclusions:The aqueous seed extract of Brassica juncea has potent hypoglycemic activity in male albino rat.

Impact of hypoxic preconditioning on apoptosis and its possible mechanism in orthotopic liver autotransplantation in rats

BACKGROUND: Hepatocyte apoptosis is a severe form of cell death after hepatic ischemia-reperfusion injury (HIRI), and its relief is an important issue in liver transplantation. Hypoxic preconditioning (HP) is considered to have protective effects on HIRI. This study was designed to explore the impact of HP on apoptosis and its possible mechanism during orthotopic liver autotransplantation. METHODS: A modified orthotopic liver autotransplantation model was used to simulate HIRI. Sprague-Dawley rats were randomly divided into normal control, autotransplantation (AT) and HP groups. The HP group was subjected to an 8% oxygen atmosphere for 90 minutes before surgery. At 1, 6 and 24 hours after surgery, the rats were killed and their liver tissue was sampled to assess the expression of Bcl-2 protein. The samples were subjected to blood chemistry study, morphological study under a light or transmission electron microscope, and quantitative study of mitochondria. RESULTS: The serum levels of ALT and AST in the HP group were lower than those in the AT group at 1, 6 and 24 hours after orthotopic liver autotransplantation (P < 0.05). Bcl-2 protein expression was increased in the HP group at each measurement point (P < 0.05). Light microscopy showed that hepatic injury in the AT group was much more severe than in the HP group. Hepatocytes in the AT group showed typical apoptosis signs under a transmission electron microscope. The ultrastructural appearance of hepatocytes in the HP group was much better than in the AT group, and the area, perimeter and diameter of the mitochondria were smaller in the HP group than in the AT group (P < 0.05). CONCLUSIONS: Hepatocytes sense and respond to decreased tissue oxygenation. Stimulation by HP relieves apoptosis by upregulating expression of Bcl-2 protein and its protection of mitochondria after orthotopic liver autotransplantation.

Effect of Hypoxic Preconditioning on Neural Cell Apoptosis and Expression of Bcl-2 and Bax in Cerebral Ischemia-Reperfusion in Rats

In order to investigate the protective effect of hypoxic preconditioning on the cerebral ischemia-reperfusion injury, the expression of Bcl-2 and Bax was detected by using immunohistochemical staining after 3 h cerebral ischemia followed by 1, 6, 12, 24 and 48 h reperfusion respectively in rats treated with or without hypoxic preconditioning before cerebral ischemia. In addition, the apoptosis of neural cells and the behavioral scores for neurological functions recovery were evaluated by TUNEL staining and ＂crawling method＂, respectively. Compared with control group （cerebral ischemia-reperfusion without hypoxic preconditioning）, the expression of Bcl-2 was significantly increased, but that of Bax decreased in the hypoxic preconditioning group （cerebral ischemiareperfusion with hypoxie preconditioning）, both P〈0.05. The pre-treatment with hypoxic preconditioning could reduce the apoptosis of neural cells and promote the neurological function recovery as compared to control group. It was suggested that hypoxic preconditioning may have protective effects on the cerebral ischemia-reperfusion injury by inhibiting the apoptosis of neural cells, increase the expression of Bcl-2 and decrease the expression of Bax.

Hypoxic preconditioning stimulates angiogenesis in ischemic penumbra after acute cerebral infarction

Previous studies have demonstrated the protective effect of hypoxic preconditioning on acute cerebral infarction, but the mechanisms underlying this protection remain unclear. To investigate the protective mechanisms of hypoxic preconditioning in relation to its effects on angiogenesis, we in- duced a photochemical model of cerebral infarction in an inbred line of mice （BALB/c）. Mice were then exposed to hypoxic preconditioning 30 minutes prior to model establishment. Results showed significantly increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra at 24 and 72 hours post infarction, mainly in neurons and vascular endothelial cells. Hypoxic preconditioning increased vascular endothelial growth factor and CD31 expression in the ischemic penumbra and the expression of vascular endothelial growth factor was positively related to that of CD31. Moreover, hypoxic preconditioning reduced the infarct volume and improved neu- rological function in mice. These findings indicate that the protective role of hypoxic preconditioning in acute cerebral infarction may possibly be due to an increase in expression of vascular endothelial growth factor and CD31 in the ischemic penumbra, which promoted angiogenesis.

Investigation of hypoglycemic,hypolipidemic and antioxidant activities of aqueous extract of Terminalia paniculata bark in diabetic rats

Objective:To investigate the hypoglycemic,hypolipidemic and antioxidant activities of aqueous extract of Terminalia paniculata bark(AETPB) in streptozotocin(STZ)-mduced diabetic rats.Methods:Acute toxicity was studied in rats after the oral administration of AETPB to determine the dose to assess hypoglycemic activity.In rats,diabetes was induced by injection of STZ(60 mg/kg,i.p.) and diabetes was confirmed 72 h after induction,and then allowed for 14 days to stabilize blood glucose level.In diabetic rats,AETPB was orally given for 28 days and its effect on blood glucose and body weight was determined on a weekly basis.At the end of the experimental day,fasting blood sample was collected to estimate the haemoglobin(Hb),glycosylated haemoglobin(HbA1c),serum creatinine,urea,serum glutamate-pyruvate transaminase(SGPT),serum glutamate-oxaloacetate transaminase(SGOT) and insulin levels. The liver and kidney were collected to determine antioxidants levels in diabetic rats.Results: Oral administration of AETPB did not exhibit toxicity and death at a dose of 2000 mg/kg.AETPB treated diabetic rats significantly(P<0.001,P<0.01 and P<0.05) reduced elevated blood glucose, HbAlc,creatinine,urea,SGPT and SGOT levels when compared with diabetic control rats.The body weight,Hb,insulin and total protein levels were significantly(P<0.001,P<0.01 and P<0.05) increased in diabetic rats treated with AETPB compared to diabetic control rats.In diabetic rats, AETPB treatment significantly reversed abnormal status of antioxidants and lipid profile levels towards near normal levels compared to diabetic control rats.Conclusions:Present study results confirm that AETPB possesses significant hypoglycemic,hypolipidemic and antioxidant activities in diabetic condition.

In vitro α-amylase inhibitory activity and in vivo hypoglycemic effect of methanol extract of Citrus macroptera Montr.fruit

Objective:To investigate the therapeutic effects of methanol extract of Citrus macroptera Montr,fruit inα-amylase inhibitory activity(in vitro)and hypoglycemic activity in normal and glucose induced hyperglycemic rats(in vivo).Methods:Fruits of Citrus macroptera without rind was extracted with pure methanol following cold extraction and tested for presence of phytochemical constituents,α-amylase inhibitory activity,and hypoglycemic effect in normal rats and glucose induced hyperglycemic rats.Results:Presence of saponin,steroid and terpenoid were identified in the extract.The results showed that fruit extract had moderateα-amylase inhibitory activity[IC_(50)value=(3.638±0.190)mg/mL]as compared to acarbose.Moreover at 500 mg/kg and 1000 mg/kg doses fruit extract significantly(P<0.05 and P<0.01 respectively)reduced fasting blood glucose level in normal rats as compared to glibenclamide(5 mg/kg).In oral glucose tolerance test,500 mg/kg dose significantly reduced blood glucose level(P<0.05)at 2 h but 1000 mg/kg dose significantly reduced blood glucose level at 2 h and 3 h(P<0.05 and P<0.01 respectively)whereas glibenclamide(5 mg/kg)significantly reduced glucose level at every hour after administration.Overall time effect is also considered extremely significant with F value=23.83 and P value=0.0001 in oral glucose tolerance test.Conclusion:These findings suggest that the plant may be a potential source for the development of new oral hypoglycemic agent.