The benzofuran norwedelic acid from Wedelia calendulaceae

A new compound norwedelic acid [5,6-dihydroxy-2(2′,4′,6′-trihydroxyphenyl)-benzofuran-3-carboxylic acid] has been isolated from fresh leaves of Wedelia calendulaceae apart from norwedelolactone, a compound previously found in Eclipta alba.     

Stimulation of Growth and Nutrient Uptake by VAM Fungi in Brassica Oleracea Var. Capitata

Cabbage (Brassica oleracea, var. capitata, cv. Hercules) seedlings were inoculated with vesicular-arbuscular mycorrhizal (VAM) fungi Glomus fasciculatum, G. aggregatum, and G. mosseae. Differential efficiency in mycorrhizal colonization and the specificity of fungal symbiont to stimulate the growth and nutrient uptake of the host were observed. In addition, there was an increase in phenol, protein, reducing sugar contents, and peroxidase activity in the VAM inoculated seedlings. Since these compounds are known to confer resistance against fungal pathogens, the use of VAM as a biological control agent to protect cabbage against several root diseases is suggested.     

Activation of the mitochondrial apoptotic pathway contributes to methotrexate‐induced small intestinal injury in rats

The efficacy of methotrexate (MTX), a commonly used chemotherapeutic drug, is limited by intestinal injury. As the mechanism of MTX‐induced small intestinal injury is not clear, there is no definitive treatment for MTX‐induced gastrointestinal injury. The present study investigates the role of mitochondrial apoptotic pathway in MTX‐induced small intestinal injury and examines whether aminoguanidine is effective in preventing the damage. Eight Wistar rats were administered 3 consecutive i.p. injections of 7 mg/kg body wt. MTX. Some rats were pretreated with 30 mg or 50 mg/kg body wt. of aminoguanidine (n = 6 in each group). Protein expressions of cytochrome c, caspases 3 and 9, and PARP‐1 were determined in the small intestines by immunohistochemistry and western blot. Mitochondrial pathway of apoptosis was activated in the small intestines of MTX‐treated rats as evidenced by intense immunostaining for cyt c, caspases 9 and 3, and PARP‐1 and mitochondrial release of cyt c, activation of caspases, and PARP‐1 cleavage by Western blot. Immunofluorescence revealed increased nuclear localization of PARP‐1. Aminoguanidine pretreatment ameliorated MTX‐induced small intestinal injury in dose‐dependent manner and inactivated the mitochondrial apoptotic pathway. Aminoguanidine may possess beneficial intestinal protective effects as an adjuvant co‐drug against MTX intestinal toxicity during cancer chemotherapy. As the mechanism of MTX‐induced small intestinal injury is not clear, there is no definitive treatment for MTX‐induced gastrointestinal injury. The results of the present study show that the mitochondrial pathway of apoptosis plays a role in MTX‐induced small intestinal injury as evidenced by cytochrome c release, activation of caspases 9 and 3, PARP‐1 cleavage, and DNA fragmentation. Aminoguanidine (AG) pretreatment attenuates the severity of small‐intestinal injury induced in rats by MTX treatment. The mechanisms of action of AG involve inhibition of iNOS, and mitochondrial pathway of apoptosis. It is suggested that aminoguanidine may possess beneficial intestinal protective effects as an adjuvant co‐drug against MTX intestinal toxicity during cancer chemotherapy.