ABSTRACT
Purpose: Repeated stress events are well known to be associated with the onset of behavioral abnormalities including depression, anxiety and memory impairment. In spite of the traditional uses of Moringa oleifera (MO), no experimental evidence for its use against chronic stress exists. Here, we investigated whether seed oil from MO (MOO) could improve behavior abnormalities of chronic stress mice induced by water-immersion restraint stress (WIRS) and the underlying mechanism. Methods: BALB/C male mice at 12 weeks of age were exposed to chronic WIRS for two weeks and divided in to four groups: normal group, WIRS group, WIRS+MOO1 group (treated with MOO at the dose of 1 mL/kg BW), and WIRS+MOO2 group (treated with MOO 2 mL/kg BW). The MOO treatment was given orally for 23 days. On day 24, we checked the behavior parameters, the plasma level of cortisol, acetylcholinesterase (AChE) activity in hippocampus, mRNA expression level of brain-derived neurotrophic factor (BDNF) and oxidative stress parameters in brain tissues. In addition, we also checked the histopathological features of the gastric mucosa wall. Results: Administration of MOO ameliorated anxiety-like, depression-like and memory impairment phenotypes in the WIRS mouse model although the plasma cortisol concentrations were comparable among the groups. Of note, MOO both in two doses could suppress the AChE activity in hippocampus tissue and ameliorated the MDA level in prefrontal cortex tissue in mice exposed to WIRS. Although only WIRS+MOO2 group could increase the mRNA expression of BDNF, the histopathological gastric mucosa wall features were improved in all MOO groups. Conclusion: Taken together, these finding suggested that MOO may have a neuroprotective effect in the mouse model of WIRS as evidenced by improving the abnormal behaviors through enhancing mRNA expression level of BDNF, inhibited AChE activity, and prevented the increase of MDA level in the brain.
ABSTRACT
Baccharis pteronioides DC has been intermittently associated with livestock poisoning in the southwestern United States. In 2004, nearly 100 cows were reported poisoned by B. pteronioides in southern New Mexico. Initial field studies and postmortem examinations found drought conditions, evidence of B. pteronioides consumption, and a reported mortality of nearly 40%. Because postmortem materials were unsuitable for further examination, plant samples were collected for feeding trials and chemical evaluation. Forty-eight Syrian hamsters (8 weeks old) were randomly divided into 4 groups and dosed with 0, 50, 100, and 200 mg of B. pteronioides for 10 days. After dosing, the hamsters were necropsied; sera were analyzed biochemically; and tissues were collected and evaluated histologically. The hamsters treated with 200 mg and several of the 100-mg animals developed anorexia and diarrhea. These animals developed multiple hemorrhagic infarcts in the liver and kidney, with severe hemorrhagic enteritis. Histologically, the higher-dosed animals had severe necrotizing vasculitis with vascular thrombosis of hepatic and renal vessels. Many glomerular capillaries contained fibrin thrombi. The superficial intestinal and colonic mucosa was necrotic, with extensive hemorrhage and proliferation of luminal bacteria. Lower-dosed animals had mild hepatocellular swelling, with proliferation of intestinal and gastric bacteria and yeast. The findings indicate that at high doses, B. pteronioides is toxic to hamsters and produces lesions that are very similar to bacterial endotoxin-produced vasculitis and infarction. Research to purify and identify the toxin, the toxic dose, and mechanism of toxicity are ongoing.
