Dihydroquercetin improves rotenone-induced Parkinsonism by regulating NF-κB-mediated inflammation pathway in rats.

This study examined the effect of dihydroquercetin (DHQ), also knofigurewn as taxifolin, on rotenone-induced Parkinsonism in rats. Male Wistar rats were administered 1.5 mg/kg rotenone for 10 days and subsequently treated with 0.25-1.0 mg/kg DHQ for 3 days followed by the assessment of parkinsonian symptoms. Brain striatal redox stress and neurochemical dysfunction markers were assessed spectrophotometrically. Histopathological evaluation of the striatum was done by hematoxylin and eosin staining technique. The expression of genes involved in the activation of NF-κB signaling pathway (IL-1ß, TNF-α, NF-κB and IκKB), and the p53 gene in the striatum were determined by RT-qPCR. DHQ attenuated parkinsonian symptoms as well as striatal redox stress, neurochemical dysfunction, and histological alterations occasioned by rotenone toxicity. Importantly, DHQ significantly suppressed the rotenone-induced upregulation of IL-1ß, NF-κB, and IκKB expression (p < 0.05) in the striatum of parkinsonian rats. DHQ demonstrated notable neurotherapeutic potential against rotenone-induced Parkinsonism in rats by improving parkinsonian symptoms (bradykinesia, catalepsy, postural instability, impaired locomotor behavior, and tremor) and neurochemical dysfunctions via modulation of genes involved in the activation of the canonical pathway of NF-κB-mediated inflammation.

Modulatory activities of polyphenols on crude acetylene-induced cardiac and hepatic dysfunctions in a rat model.

Exposure to crude acetylene can occur in occupational settings. This study assessed the modulatory activities of selected polyphenols on the hematotoxic, cardiotoxic, and hepatotoxic effects of crude acetylene. Wistar rats were exposed to 58 000 ppm crude acetylene for 10 min at 12 h intervals for 30 days. Some exposed groups were treated with 50 mg/kg rutin, quercetin, gallic acid, or tannic acid. Indices of hematological disorder, oxidative stress, and cardiovascular and hepatocellular injuries were evaluated in animals. The results showed a decrease in the levels of hematological indices in crude acetylene-exposed animals except for white blood cell count which was increased. Decreased activity/level of reduced glutathione, superoxide dismutase and ferric reducing antioxidant power with increased lipid peroxidation was observed in animals exposed to crude acetylene. Activities of transaminases, γ-glutamyl transpeptidase, and level of bilirubin were increased while the plasma albumin level was decreased. Dyslipidemia, increased activities of lactate dehydrogenase and creatine kinase-MB, and severe histopathological damage to hepatic and cardiac tissues were also observed in animals exposed to the gas. These deleterious hematological, biochemical, and histopathological changes were ameliorated in crude acetylene-toxified rats treated with the polyphenols. Tannic acid exhibited better activity than gallic acid while quercetin showed a superior activity to rutin. The results indicate that exposure to crude acetylene can lead to blood, heart, and liver-related diseases and dietary polyphenols could provide protective benefits.

Prophylaxis with a multicomponent nutraceutical abates transient cerebral ischemia/reperfusion injury.

The effect of a multicomponent nutraceutical on cerebral ischemia/reperfusion injury in male Wistar rats was investigated. Animals were administered with the nutraceutical, Trévo™, for 7 days before 30 min of bilateral common carotid artery occlusion-induced cerebral ischemia and 24 hr of reperfusion. Behavioral assessment, biochemical estimations in the brain cortex, striatum, and hippocampus, and hippocampal histopathological evaluation were carried out after treatments. Results showed that ischemia/reperfusion-induced motor and cognitive deficits were abated in rats pretreated with Trévo™. Additionally, prophylaxis with Trévo™ blunted ischemia/reperfusion-induced redox stress, proinflammatory events, disturbances in neurotransmitter metabolism, mitochondrial dysfunction, and histoarchitectural aberrations in the discreet brain regions. In summary, supplementation with Trévo™ provided neuroprotection to rats against transient cerebral ischemia/reperfusion injury and could be explored as a promising approach in stroke prevention. PRACTICAL APPLICATIONS: There is a worldwide increase in the incidence of cerebral ischemia or stroke. Although an advanced health care system and effective control of risk factors have led to the declining incidence in developed nations, a definitive cure for stroke remains elusive and the situation is growing worse in developing nations. The results of the present study revealed that supplementation with Trévo™ ameliorated neurobehavioral, neurochemical, and histopathological consequences of brain ischemia/reperfusion injury and could, therefore, be beneficial in stroke prevention and management.

Angiotensin-1-converting enzyme inhibition, antioxidant activity, and modulation of cerebral Na+/K+ ATPase by free phenolics of African locust bean (Parkia biglobosa).

AIMS: To investigate the antioxidant activities and effects of free phenols (FPPB) and bound phenols (BPPB) of Parkia biglobosa leaves on some enzymes of neuro-cardiovascular relevance. METHODS AND RESULTS: HPLC-DAD fingerprinting of FPPB and BPPB, and the antihemolytic, radical (1,1-diphenyl-2 picrylhydrazyl, DPPH; 2,2-azino-bis(3-ethylbenzthiazoline-6-sulphonic acid), ABTS) scavenging and ferric reducing antioxidant properties of extracts, were assessed. In addition, the effects of the phenolics on angiotensin-1-converting enzyme (ACE), cerebral acetylcholinesterase/butyrylcholinesterase (AChE/BuChE), and Na+/K+ATPase were determined in vitro. FPPB was more potent than BPPB in terms of ABTS (EC50:4.06 ± 0.3 vs 24.07 ± 2.1 µg/mL) and DPPH (EC50:3.82 ± 0.2 vs 10.22 ± 0.1 µg/mL) radicals scavenged, respectively. The free phenolic extract was a better DPPH. scavenger than ascorbic acid (EC50 = 12.58 ± 0.4 µg/mL; DPPH reference) and compared well with Trolox (EC50:4.44 ± 0.08 µg/mL; ABTS reference). The anti-hemolytic effect of FPPB (36%) and BPPB (53%) was highest at 15 µg/mL but lower than that recorded for ascorbic acid (67% at 10 µg/mL). Even though FPPB (IC50 = 15.35 ± 4.0 µg/mL) and BPPB (IC50 = 46.85 ± 3.3 µg/mL) showed considerably lower ACE-inhibitory effect than ramipril (IC50:0.173 ± 0.04 µg/mL), both extracts demonstrated dose-dependent, significant (p < 0.01/p < 0.05) inhibition of the enzyme. FPPB increased cerebral Na+/K+ATPase activity but neither phenolic extract affects cerebral AChE/BuChE activities. HPLC-DAD revealed catechin, caffeic acid, and quercetin, respectively, as the major phenolics (mg/g) in FPPB (29.85, 30.29, and 17.10) and BPPB (32.70, 30.51, and 19.25). CONCLUSION: The effects of P biglobosa on ACE and cerebral ATPase are related to its constituent phenolics. ACE inhibition could be an important mechanism underlying the documented hypotensive effect of the plant.

Antioxidant and antiulcer potential of aqueous leaf extract of Kigelia africana against ethanol-induced ulcer in rats.

Ethnobotanical claims regarding Kigelia africana reported antiulcer properties as part of its medicinal application. In this work, aqueous leaf extract from K. africana was investigated for its phytochemical constituents and antiulcer potential against ethanol-induced ulcer in rats. The participation of oxidative stress on ethanol-induced ulcer and the potential protective antioxidant activity of K. africana extracts were investigated by determining vitamin C and thiobarbituric acid reactive species (TBARS) contents in the gastric mucosa of rats. The HPLC analysis showed the presence of gallic acid, chlorogenic acid, caffeic acid and also the flavonoids rutin, quercetin and kaempferol in the aqueous plant extract. Oral treatment with K. africana extract (1.75; 3.5; 7 and 14 mg/kg) one hour after ulcer induction with ethanol decreased in a dose dependent manner the ulcer index. Ethanol increased significantly stomachal TBARS levels and decreased vitamin C content when compared to the control animals. K. africana blunted the ethanol-induced oxidative stress and restored vitamin C content to the control levels. The present results indicate that the aqueous leaf extract from K. africana possesses antiulcer potential. The presence of flavonoids in plant extract suggests that its antiulcerogenic potential is associated with antioxidant activity. Of particular therapeutic potential, K. africana was effective against ethanol even after the induction of ulcer, indicating that it can have protective and curative effects against gastric lesion.