2 research outputs found
Synthesis, anti-inflammatory and analgesic activity of 2-[4-(substituted benzylideneamino)-5-(substituted phenoxymethyl)-4H-1,2,4-triazol-3-yl thio] acetic acid derivatives
AbstractThe title compounds 3a–l have been synthesized by the reaction of thiocarbohydrazide with substituted phenoxy acetic acid to obtained substituted 1,2,4-triazoles (1). Compound 1 was treated with various substituted aromatic aldehydes which results in 4-(substituted benzylideneamino)-5-(substituted phenoxymethyl)-2H-1,2,4-triazol-3(4H)-thiones (2a–g), further 2a–g is converted to 2-[4-(substituted benzylideneamino)-5-(substituted phenoxymethyl)-4H-1,2,4-triazol-3-yl thio] acetic acid (3a–l) derivatives by the reaction with chloroacetic acid. All the newly synthesized compounds were evaluated for in vivo anti-inflammatory and analgesic activities. Among the series 2-[4-(2,4-dichlorobenzylideneamino)-5-(phenoxymethyl)-4H-1,2,4-triazol-3-yl thio] acetic acid (3d), 2-[4-(4-dichlorobenzylideneamino)-5-(phenoxymethyl)-4H-1,2,4-triazol-3-yl thio] acetic acid (3e), 2-[4-(2,4-dichlorobenzylideneamino)-5-[(2,4-dichlorophenoxy)methyl]-4H-1,2,4-triazol-3-yl thio] acetic acid (3j) and 2-[5-[(2,4-dichlorophenoxy)methyl)]-4-(4-chlorobenzylideneamino)-4H-1,2,4-triazol-3-yl thio] acetic acid (3k) showed significant anti-inflammatory activity with P<0.001 (63.4%, 62.0%, 64.1% and 62.5% edema inhibition, respectively), as compared to the standard drug diclofenac (67.0%) after third hour respectively and also compounds 3j, 3k exhibited significant analgesic activity with P<0.001 (55.9% and 54.9% protection, respectively) and less ulcerogenic activity as compared with standard drug aspirin (57.8%)
Cardioprotective effect of ascorbic acid on doxorubicin-induced myocardial toxicity in rats
Objective : To investigate the preventive and curative role of ascorbic
acid on doxorubicin (dox)-induced myocardial toxicity in rats.
Materials and Methods : Animals were divided into five groups of six
animals each. Group I served as normal control and received saline 5
ml/kg/day intraperitoneal (i.p.) for a period of 15 days. Group II
animals received ascorbic acid 20 mg/kg per oral (p.o.) for 15 days as
a pretreatment control (PR). Group III animals received dox 2.5 mg/kg
body weight (b.w.), i.p., in six equal injections for two weeks for a
total cumulative dose of 15 mg/kg b.w. Group IV animals received
ascorbic acid 20 mg/kg p.o. for 15 days as a pretreatment followed by
dox 2.5 mg/kg b.w., i.p., in six equal injections for two weeks for a
total cumulative dose of 15 mg/kg body weight. Group V animals received
dox 2.5 mg/kg b.w., i.p., in six equal injections for two weeks for a
total cumulative dose of 15 mg/kg b.w. followed by ascorbic acid 20
mg/kg p.o for 15 days as post-treatment control (CR). The biochemical
parameters such as tissue glutathione (GSH), malondialdehyde (MDA),
catalase (CAT), and superoxide dismutase (SOD), and enzyme biomarkers
such as creatine phosphokinase (CPK), lactate dehydrogenase (LDH),
aspartate aminotransferase (AST), and alanine aminotransferase (ALT)
were monitored. Results : Pretreatment with ascorbic acid (20 mg/kg
p.o.) significantly protected the myocardium from the toxic effect of
dox (PR), by increasing the levels of antioxidant enzymes such as GSH,
SOD, and CAT toward normal and decreased the levels of MDA, CPK, LDH,
AST, and ALT as compared with dox-treated rats. Post-treatment with
ascorbic acid to dox-treated group (CR) significantly increased the
levels of tissue GSH, SOD, CAT and significantly decreased the level of
MDA as compared with dox-treated group. It also reduced the severity of
cellular damage of the myocardium as confirmed by histopathology. The
restoration of the endogenous antioxidant system clearly depicts that
ascorbic acid produced its protective effect by scavenging the reactive
oxygen species. Conclusion : The results obtained in this study provide
evidence for the usefulness of the ascorbic acid as a cardioprotective
agent