Bombax Costatum extract abrogates piroxicam-mediated hepatic and gastric toxicities in rats.

OBJECTIVE: Concurrent administration of orthodox drugs and herbs is common in tropical Africa. This study investigates the effect of co-administration of piroxicam and Bombax costatum on hepatic and gastric toxicities and levels of oxidative stress markers. MATERIALS AND METHODS: Twenty male wistar rats were grouped into four. Rats in group one were administered 1mL/kg distilled water as normal control; group two were treated with 400mg/kg of extract; group three were treated with 20mg/kg of piroxicam; while those in group four were treated with both extract and piroxicam at 400mg/kg and 20mg/kg, respectively. All treatments were given orally for 14 days. At the end of the treatment period, the rats were euthanised; blood samples and stomach were collected for determination of hepatic and gastro-toxicity alongside with oxidative stress markers. RESULTS: Treatment with piroxicam alone shows the presence of oxidative stress with marked hepatic and gastric toxicities. Oxidative stress markers, hepatic and gastric toxicity indices after treatment with extract alone and in combination with piroxicam appear like that of the control group. CONCLUSION: Concurrent administration of piroxicam and Bombax costatum prevents piroxicam-induced hepatic and gastric toxicities with a positive effect on antioxidant levels. This may indicate important health benefits of this drug-herb combination.

Anti-inflammatory activity and gastric lesions induced by zinc-tenoxicam.

Oral administration of tenoxicam or zinc-tenoxicam complex inhibited to a similar extent carrageenin-induced paw oedema and granulomatous tissue formation in rats as well as the acetic acid induced writhing response in mice. Gastric lesions induced by oral administration of zinc-tenoxicam were reduced in number and severity when compared with those induced by tenoxicam or the co-administration of tenoxicam and zinc acetate. However, after intraperitoneal administration, both zinc-tenoxicam and tenoxicam plus zinc acetate induced a reduced number of gastric lesions as compared with tenoxicam.

Prostaglandin E(2) protects intestinal tumors from nonsteroidal anti-inflammatory drug-induced regression in Apc(Min/+) mice.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are antitumorigenic in humans as well as in animal models of intestinal neoplasia, such as the adenomatous polyposis coli (Min/+) (Apc(Min/+)) mouse. NSAIDs inhibit cyclooxygenase (COX) isozymes, which are responsible for the committed step in prostaglandin biosynthesis, and this has been considered the primary mechanism by which NSAIDs exert their antitumorigenic effects. However, mounting evidence suggests the existence of COX-independent mechanisms. In the present study, we attempted to clarify this issue by treating Apc(Min/+) mice bearing established tumors with NSAIDs (piroxicam and sulindac, 0.5 and 0.6 mg/mouse/day, respectively) for 6 days and concomitantly bypassing COX inhibition by treatment with the E prostaglandin (EP) receptor agonists 16,16-dimethyl-prostaglandin E(2) (PGE(2)) and 17-phenyl-trinor-PGE(2) (10 microg each, three times daily) administered via gavage and/or i.p. routes. Treatment with piroxicam and sulindac resulted in 95% and 52% fewer tumors, respectively, and a higher ratio of apoptosis:mitosis in tumors from sulindac-treated mice as compared with controls. These effects were attenuated by concomitant EP receptor agonist treatment, suggesting PGE(2) is important in the maintenance of tumor integrity. Immunological sequestration of PGE(2) with an anti-PGE(2) monoclonal antibody likewise resulted in 33% fewer tumors in Apc(Min/+) mice relative to untreated controls, additionally substantiating a role for PGE(2) in tumorigenesis. The EP receptor subtype EP1 mediates the effects of PGE(2) by increasing intracellular calcium levels ([Ca(2+)](i)), whereas antagonism of EP1 has been shown to attenuate tumorigenesis in Apc(Min/+) mice. We demonstrate that [Ca(2+)](i) is significantly elevated in tumors of Apc(Min/+) mice relative to the adjacent normal-appearing mucosa. Furthermore, treatment with piroxicam results in significantly lower [Ca(2+)](i) in tumors, and this effect is attenuated by concomitant treatment with the EP1/EP3 receptor agonist 17-phenyl-trinor-PGE(2). Overall, our results suggest that NSAIDs exert their antitumorigenic effects, in part, via interference with PGE(2) biosynthesis, and these effects may be mediated through changes in intracellular calcium levels.

[In vitro effects of L-carnitine on the inhibition of sperm mobility induced by FANS]. / Effetti "in vitro" della L-Carnitina sulla inibizione della motilità degli spermatozoi indotta da F.A.N.S.

OBJECTIVE: We wanted to study the function of some substances present in the seminal fluid (PG and L. Carnitine), which, with different mechanisms, affected Spermatozoa motility, and to study the effect of other substances (F.A.N.S.), known also for their action on P.G. PATIENTS AND METHODS: Ten samples of seminal fluid from healthy subjects were studied according to the indications of the World Health Organization (1992). RESULTS: All the F.A.N.S. used (Cinnoxicam, Salicylic Acetyl Acid) had an inhibitory effect on motility, as did L. Carnitine at high doses. We thought it interesting to observe if L. Carnitine added to the seminal fluid before F.A.N.S. blocked their effects. CONCLUSIONS: The pre-treatment with L. Carnitine had an "in vitro" buffering effect on F.A.N.S.

[Protective effect of ranitidine in the stomach and duodenum against piroxicam. An endoscopy controlled double-blind study]. / Schutzwirkung von Ranitidin in Magen und Duodenum gegenüber Piroxicam. Eine endoskopisch kontrollierte Doppelblindstudie.

Protective Effects of Ranitidine in Stomach and Duodenum against Piroxicam / An endoscopically controlled double-blind study In a randomized parallel double-blind study the gastroduodenal effects of 20 mg piroxicam (CAS 36322-90-4) daily in the presence and absence of 300 mg ranitidine nocte was evaluated in 28 healthy volunteers undergoing upper gastrointestinal endoscopy. Drugs were taken over a period of 14 days. Endoscopic controls were performed at entry, and repeated after 7 and 14 days of treatment. A damaging score according to Lanza et al. was used. At entry, both groups displayed comparable mucosal damages in the stomach (0.9 +/- 0.1) and in the duodenum (0.4 +/- 0.2). After 14 days the mean lesion score increased in the piroxicam/placebo group to 6.3 +/- 1.6 in the stomach and to 4.0 +/- 1.4 in the duodenum. The corresponding values in the piroxicam/ranitidine group were 3.4 +/- 1.0 (stomach) and 0.4 +/- 0.2 (duodenum). This protection afforded by ranitidine was significant when compared with placebo (p < 0.05). Our data suggest that 300 mg ranitidine at night markedly protect the stomach and the duodenum against piroxicam.