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Biomedical subjects

K K Saxena

Publications and source records attributed to K K Saxena.

At least 19 recordsLinked to original sources

Synthesis and anticonvulsant activity of some potential thiazolidinonyl 2-oxo/thiobarbituric acids.

A series of 5-[(N-substituted benzylidenylimino)amino]-2-oxo/thiobarbituric acids (3a-3h) have been synthesized by the condensation of 5-hydrazino-2-oxo/thiobarbituric acids (2a-2b) with various aromatic aldehydes. Cycloaddition of thioglycolic acid to 3a-3h, yielded 5-[(2'-substituted phenyl-4'-oxothiazolidin-3'-yl)amino]-2-oxo/thiobarbituric acids (4a-4h). All these compounds were screened, in vivo, for their anticonvulsant activity and acute toxicity studies. Compounds 4f and 4g were found to be most potent compounds of this series and were compared with the reference drugs, phenytoin sodium, lamotrigine and sodium valproate. The structures of these compounds have been established by IR, 1H NMR and mass spectroscopic data.

Animals↗

A study of anti-inflammatory activity of some novel alpha-amino naphthalene and beta-amino naphthalene derivatives.

In the present study, some naphthalene derivatives have been synthesized by incorporating azetidinyl and thiazolidinyl moieties at its alpha- or beta-positions such as alpha-(3-chloro-2-oxo-4-substituted)aryl-1-azetidinyl)naphthalenes 6-10, alpha-((substituted)aryl-4-oxo-1,3-thiazolidin-3-yl)naphthalenes 11-15, beta-(3-chloro-2-oxo-4-substituted aryl-1-azetidinyl)naphthalenes 21-25, and beta-(substituted aryl-4-oxo-1,3-thiazolidin-3-yl)naphthalenes 26-30. These compounds have also been screened for acute toxicity and anti-inflammatory and analgesic activities. Compounds which showed better anti-inflammatory and analgesic activities were also examined for their ulcerogenic liability and underwent a cyclooxygenase assay. Two compounds, 12 and 28, were found to exhibit potent anti-inflammatory activity as compared to the standard drugs phenylbutazone and naproxen.

Analgesics↗

Hepatoprotective activity of Beta vulgaris against CCl4-induced hepatic injury in rats.

Ethanolic extract of Beta vulgaris roots given orally at doses of 1000, 2000 and 4000 mg/kg exhibited significant dose-dependent hepatoprotective activity against carbontetrachloride (CCl(4))-induced hepatotoxicity in rats. Hepatotoxicity and its prevention were assessed by serum markers viz. cholesterol, triglyceride, alanine amino transferase and alkaline phosphatase.

Alkaline Phosphatase↗

Topical amiloride solution accelerates healing of mechanical skin ulcers in albino rats.

The present investigation was undertaken to explore the ulcer healing properties of three dosage schedules of various concentrations of topically administered amiloride solution in mechanically produced skin ulcers in albino rats. Four skin ulcers (two on either side of the midline) were made 2.5 cm apart on the preshaved back of each anesthetized rat with a round body skin biopsy punch (7 mm diameter) through the dermis to the depth of subcutaneous tissue. The animals were randomly divided into groups of 5 rats each. Ulcers on one side of the midline were treated with normal saline and served as control, whereas those on the other side were treated with amiloride solutions. Each ulcer was observed for its size, slough formation and any sign of irritation on alternate days until healing was complete. Healing of ulcers was significantly accelerated with all the strengths of amiloride (0.01, 0.02 and 0.04%) in all the dosage schedules (o.d., b.i.d. and q.i.d.) in terms of days required for complete healing, ulcer size and area under the size-time curve. This acceleration was dose-dependent with maximum effect at b.i.d. administration of 0.04% solution. No irritation or suppression of immunity was noticeable. Thus topical amiloride may prove to be an inexpensive and better ulcer healing agent with no apparent side effects. Inhibition of u-PA by amiloride seems to be responsible for this effect.

Administration, Topical↗

Beneficial effects of Allium sativum, Allium cepa and Commiphora mukul on experimental hyperlipidemia and atherosclerosis--a comparative evaluation.

Oral administration of petroleum ether extract of Allium sativum, Allium cepa and ethylacetate extract of Commiphora mukul in albino rats significantly prevented rise in serum cholesterol and serum triglyceride level, caused by atherogenic diet. All the three agents were also found to confer significant protection against atherogenic diet induced atherosclerosis.

Allium↗

Effect of pinealectomy on daily rhythm of blood glucose in rabbits.

Daily rhythm of blood glucose was studied in superior cervical ganglionectomized (SCGX), sham operated and normal rabbits. A typical daily rhythm was observed in normal animals which was not influenced by surgical procedures. However, ganglionectomy, which tantamount to physiological elimination of pineal gland, caused complete reversal of this rhythm. Probable role of pineal gland in controlling blood glucose daily rhythm is suggested.

Animals↗

Modification of glybenclamide hypoglycaemia by verapamil in rabbits.

The study was designed to demonstrate the interaction between verapamil and glybenclamide on blood glucose in rabbits. Glybenclamide (0.05 mg/kg, po) induced hypoglycaemia was observed 1 h after treatment and persisted till 3 h. Verapamil (8 mg/kg, sc) per se produced hyperglycaemia which lasted for 2 1/2 hr. Concurrent administration of verapamil was found to impair significantly the hypoglycaemic response of glybenclamide.

Animals↗

Effect of cambendazole and haloxon on the carbohydrate metabolism of Ascaridia galli and Heterakis gallinae (Nematoda).

Cambendazole 10(-4) M significantly reduced the level of glycogen in both the parasites. Lactic acid level was found enhanced. Oxygen consumption was suppressed by 63 and 94% in A. galli and H. gallinae, respectively, by 10(-4) M cambendazole. Haloxon did not cause any significant change in glycogen and lactic acid level in either parasite, but reduced oxygen consumption by 23 and 31% in Ascaridia galli and Heterakis gallinae, respectively.

Animals↗

The effect of levamisole and albendazole on some enzymes of Ascaridia galli and Heterakis gallinae.

Ascaridia galli and Heterakis gallinae obtained from the common fowl Gallus gallus were exposed to 10(-2)-10(-5)M levamisole and albendazole; both compounds caused death of the parasites in vitro. The effect of the drugs was investigated on homogenates of the treated worms. Albendazole, at 10(-2)M, inhibited oxaloacetate reduction by 67 and 53% and malate oxidation by 21 and 17% in A. galli and H. gallinae, respectively, whereas 10(-4)M levamisole completely inhibited malate dehydrogenase activity in both directions in the two parasites. Lactate dehydrogenase was not affected significantly by either anthelmintic. Aldolase activity was diminished by 57 and 32% in A. galli and H. gallinae, respectively, with 10(-4)M levamisole. Levamisole at 10(-4)M also inhibited the activity of acid and alkaline phosphomonoesterase and cholinesterase. Albendazole had no significant effect on these enzymes in either parasite. Malate dehydrogenase and cholinesterase activity of the host tissue (intestine and caecum) was also reduced significantly with 10(-2) and 10(-3)M levamisole. These studies indicated a multiple mode of action of levamisole and albendazole.

Albendazole↗

Effect of parbendazole and piperazine adipate on the activity of some enzymes of Ascaridia galli and Heterakis gallinae.

Adult Ascaridia galli and Heterakis gallinae obtained from the fowl (Gallus gallus) were treated in vitro with 10(-2) to 10(-5) M parbendazole and piperazine adipate for 10-60 min at 38 degrees C. Both the compounds at 10(-2) M caused mortality of A. galli and H. gallinae after a maximum of 30 min exposure. The effect of the drugs on the homogenates of the treated worm was investigated. Parbendazole (10(-2) M) inhibited malate oxidation by 68% in A. galli and 62% in H. gallinae. Piperazine adipate (10(-2) M) inhibited malate oxidation by 78% in both parasites. In A. galli oxaloacetate reduction was inhibited by 41 and 26% by 10(-2) M parbendazole and piperazine adipate, respectively; with H. gallinae this inhibition was found to be 39 and 55%, respectively. Aldolase activity in both the parasites was also inhibited by 10(-2) M parbendazole and piperazine adipate. Both compounds caused an inhibition of acid phosphomonoesterase activity, but the activities of lactate dehydrogenase and alkaline phosphomonoesterase were not affected significantly. Parbendazole (10(-2) M) had no significant effect on the cholinesterase activity of these parasites, but piperazine adipate (10(-2) M) caused an inhibition of 96% in A. galli and 93% in H. gallinae. The possible mode of action of the drugs is discussed.

Acid Phosphatase↗

The effect of piperazine adipate and parbendazole on the carbohydrate metabolism of Ascaridia galli and Heterakis gallinae.

Carbohydrate metabolism of Ascardia galli and Heterakis gallinae was studied after their exposure in vitro to 10(-2) to 10(-5) M piperazine adipate and parbendazole for 10 to 60 min. Following treatment with 10(-2) M piperazine adipate O2 uptake was reduced by 87% in A. galli and 70% in H. gallinae, while parbendazole (10(-2) M) reduced O2 uptake by 70% and 86%, respectively. Glycogen contents were reduced significantly by 10(-2) M piperazine adipate in both the worms, while lactic acid level was enhanced. Parbendazole, however, did not cause any significant change in glycogen contents and lactic acid level in either parasite.

Animals↗

Effect of some anthelmintics on malate dehydrogenase activity and mortality in two avian nematodes Ascaridia galli and Heterakis gallinae.

Cambendazole and tiabendazole at 10(-4) M concentrations caused mortality in both the parasites after 10 min and 20 min, respectively. H. gallinae was killed by 10(-4) M haloxon but A. galli remained alive even after 60 min exposure. The effect of these drugs was found to be irreversible since no resumption of activity was observed when the parasites were returned to normal saline solution. The ratio of oxaloacetate reduction to malate oxidation in the homogenates of A. galli and H. gallinae was 4.38:1 and 3.17:1 respectively. Cambendazole at 10(-3) M inhibited the enzymic activity in both directions by 100% in both A. galli and H. gallinae. 10(-3) M tiabendazole, however, inhibited the malate oxidation by 82.8 and 60.8% and oxaloacetate reduction by 76.6 and 92% in A. galli and H. gallinae, respectively. Haloxon had little effect on malate dehydrogenase activity of any of the parasite. Assay of malate dehydrogenase, following the in vitro drug treatment cambendazole and tiabendazole, exhibited moderate inhibition of the activity in both the parasites.

Animals↗