“…Peroxynitrite (ONOO)toxicity is involved in neurodegenerative and inflammatory diseases such as PD. Alaternin isolated from this plant has potent ONOOscavenging activity and anti-inflammatory property, which makes it a suitable candidate for PD [60].…”
Section: Cassia Obtusifolia Cassiae Semen or Cassia Toramentioning
Parkinson's disease (PD) is a neurodegenerative disorder due to dopamine deficit in substatia nigra. PD is mainly a sporadic disease with unestablished etiology. However, exposure to environmental toxins, head trauma, inflammation, and free radicals are potential reasons. Recently, the role of oxidative stress in neurological abnormalities, including PD, has been particularly addressed. Antioxidant remedies, particularly herbal antioxidants, have revealed new perspectives of research and therapy as possible preventive and therapeutic approaches for PD. In this paper, we reviewed the recently published papers on the effects of herbal medicines on PD alongside the pathogenesis of PD with regard to oxidative stress.
“…Peroxynitrite (ONOO)toxicity is involved in neurodegenerative and inflammatory diseases such as PD. Alaternin isolated from this plant has potent ONOOscavenging activity and anti-inflammatory property, which makes it a suitable candidate for PD [60].…”
Section: Cassia Obtusifolia Cassiae Semen or Cassia Toramentioning
Parkinson's disease (PD) is a neurodegenerative disorder due to dopamine deficit in substatia nigra. PD is mainly a sporadic disease with unestablished etiology. However, exposure to environmental toxins, head trauma, inflammation, and free radicals are potential reasons. Recently, the role of oxidative stress in neurological abnormalities, including PD, has been particularly addressed. Antioxidant remedies, particularly herbal antioxidants, have revealed new perspectives of research and therapy as possible preventive and therapeutic approaches for PD. In this paper, we reviewed the recently published papers on the effects of herbal medicines on PD alongside the pathogenesis of PD with regard to oxidative stress.
“…In line with inflammation in ischemic brain, glial cells including microglia and astrocytes are also involved in neuronal degeneration (Petito et al, 1990;Denes et al, 2007). Based on these observations, many drugs have been tested for their abilities to delay neuronal death, including cyclooxygenase-2 inhibitors (Gackowski et al, 2008;Hamel et al, 2008), nuclear factor-B inhibitors (Ridder and Schwaninger, 2009), inducible nitric oxide synthase inhibitors (Cai et al, 2008;Shin et al, 2010), 0378 and inhibitors against glial cell activation (Muramatsu et al, 2004;Lee et al, 2011). However, when selective anti-inflammatory or anti-excitatory agents were applied in ischemic brain damage, satisfactory outcomes were not obtained (Guo et al, 2009).…”
“…Another study by Dal-Pan and colleagues (2017) showed that high polyphenol concentrations in berries could prevent neuropathological damage and cognitive impairment in an animal model of Alzheimer's disease. In our study, only changes that took place within the first 7 days post-surgery were reported although neuronal death and associated neurobehavioural deficits are known to occur months after I/R-induced injury (Shin et al 2010). The potential role of FRHT and other botanicals in post-stroke recovery especially in terms of improvements in cognitive and motor impairments, require further investigation.…”
Stroke is the second leading cause of death worldwide, affecting about 240 people a day in South Africa and leaving survivors with residual disabilities. At the moment, there is no clinically approved neuroprotective product for stroke but the consumption of plant polyphenols has been suggested to offer some protection against stroke. In this study, we investigated the effects of long-term consumption of fermented rooibos herbal tea (FRHT) on ischemia/reperfusion (I/R)-induced brain injury in adult male Wistar rats. FRHT was administered to the animals ad libitum for 7 weeks prior to the induction of ischemic injury via a 20-minute bilateral occlusion of the common carotid arteries (BCCAO) followed by reperfusion for 24, 96 and 168 hours respectively. Neurobehavioural deficits, brain oedema, blood-brain barrier (BBB) damage, apoptosis, lipid peroxidation and total antioxidant capacity were subsequently evaluated using standard methods. Our results showed that long-term consumption of FRHT by Wistar rats significantly reduced brain oedema and neuronal apoptosis, but did not attenuate BBB damage following cerebral ischemia. Analysis of whole-brain homogenates showed significantly reduced lipid peroxidation levels, increased total antioxidant capacity and resulted in improved neurobehavioural outcomes in FRHT-treated rats when compared with untreated animals. Taken together, our results tend to suggest that continuous consumption of FRHT could confer some protection against ischemic brain injury (IBI) and is therefore highly recommended for patients with stroke-predisposing conditions.
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