<p><em>Smilax zeylanica </em>Linn has been traditionally used in the treatment of rheumatoid arthritis but, no scientific data has been published supporting the claimed ethanomedical use. This study was designed to investigate the immunomodulatory and antiarthritic activities of <em>Smilax zeylanica</em>.</p><p>Methanolic extract of <em>Smilax zeylanica </em>(MESZ) roots was tested for its immunomodulatory activity by NBT reduction test. Antiarthritic activity of the same was tested by <em>in vitro </em>protein denaturation and <em>in vivo </em>complete Freunds adjuvant (CFA) induced arthritis.<strong> </strong></p><p>MESZ<strong> </strong>showed its significant effect on both cell mediated and humoral immunity to suppress stimulated immune responses in NBT reduction test . It also markedly inhibited protein denaturation in <em>in vitro </em>model. Extract at 200 mg/kg and 400 mg/kg showed statistically significant inhibition ( p<0.05) of the edema formation in CFA model. Histopathological studies of ankle joints also supported this finding.</p>The presence of steroids in the extract might be responsible for the prominent immunomodulatory and antiarthritic activities of the plant. Hence the present study concluded that <em>Smilax zeylanica</em> holds immunomodulatory and antiarthritic activities.
Aging is associated with suppressed endothelial cell (EC) autophagy and EC nitric oxide (NO) bioavailability. A link might exist among autophagy, mitophagy, and stimulated NO production in ECs. ECs treated with scrambled siRNA exposed to shear stress (3 h x 20 dyn/cm2) exhibit: ↑LC3‐II:LC3‐1, ↓p62, ↑LC3‐GFP puncta formation (indices of increased autophagy); ↓VDAC, ↓m‐aconitase, ↑TOM20:LAMP1 colocalization, ↓ mitochondrial pH indicating lysosomal compartmentalization (indices of increased mitochondrial turnover), ↑ROS generation, ↑endothelial NO synthase (eNOS) phosphorylation, and ↑NO production (p<0.05 for all). ECs transfected with AuTophaGy‐related protein 3 (Atg3) siRNA did not exhibit shear‐induced autophagy, mitochondrial turnover, eNOS phosphorylation, or NO production, but ROS accumulation and cytokine production (ICAM‐1, MCP‐1, IL‐8, E‐selectin) were exaggerated (all p<0.05). Shear‐induced increases in oxygen consumption rate, extracellular acidification rate, and ATP production (all p<0.05) in ECs were prevented by autophagy suppression, indicating impaired mitochondrial function. Dysfunctional mitochondria might be the source of ROS when autophagy is compromised because: (i) shear‐induced increases in NO generation were restored, and ROS production and inflammation were normalized, when ECs +Atg3 siRNA were treated with a mitochondrial‐targeted O2•‐ scavenger; and (ii) the EC phenotype +Atg3 siRNA could be recapitulated using approaches that limit mitophagy per se. A crosstalk exists among autophagy, mitophagy, and NO production in ECs.
Rheumatoid arthritis is a systemic disease that causes progressive joint damage and disability. The macrophage is an important pathogenic mediator in rheumatoid arthritis, and cytokines such as tumour necrosis factor alpha (TNFα) and interleukin-1 are therapeutic targets. Drugs that block TNF a decrease joint inflammation and slow radiographic progression. There are various strategies for treatment of rheumatoid arthritis such as Allopathy, Homeopathy, Ayurveda etc. In this review we discussed about the potency and side effects of various treatment approaches of RA. Allopathy is a first line of treatment especially in acute conditions which provides both symptomatic and root cause relief. But it is supplemented with an array of side effects which limits their use chronically. It can also be cured through Complementary and Alternative Medicine (CAM) like yoga, Ayurveda, Naturopathy, Homeopathy, Unani, Siddha, acupuncture, etc. which has enough potential and remedial measures in treating arthritis. Home remedies, preventions and precautions are also important aspects in minimizing the effect of arthritis.
We hypothesized that biological metabolites of quercetin, resveratrol, and grape seed extract previously identified in human plasma can prevent impairment of nitric oxide (NO) bioavailability due to glucotoxic conditions (e.g. Type 1 or 2 diabetes). Human aortic endothelial cells were treated for 24 h with 2μΜ Quercetin‐3‐O‐glucoronide, 5μΜ Piceatannol, or 1μΜ 3‐Hydroproponoic acid. Cells were next exposed to normal (5mM) or high (25mM) glucose for 48h, then treated with insulin (100nM, 10 min) to stimulate NO production. In the absence of polyphenols, insulin stimulation increased (P<0.05) indices of NO production, phosphorylated to total Akt (p‐AktSer473:Akt), and endothelial nitric oxide synthase (p‐eNOSser1177:eNOS) in cells grown in 5mM but not 25mM glucose. Pretreatment of cells with polyphenol metabolites prior to 25mM glucose exposure preserved insulin stimulated increases (P<0.05) in NO, p‐AktSer473:Akt and p‐eNOSser1177:eNOS. These effects may be secondary to oxidative stress as elevations (P<0.05) in reactive oxygen and nitrogen species in cells treated with 25mM glucose were completely prevented by all polyphenol metabolites. These data indicate that biological metabolites of quercetin, resveratrol, and grape seed extract protected against gluocotoxic impairment of insulin dependent NO bioavailability, and preserved the insulin ‐ Akt ‐ eNOS signaling axis.
The vascular benefits of anthocyanins might be mediated by their circulating metabolites. This mechanism has not been explored because the metabolites are not commercially available. We synthesized the blueberry (BB) metabolites vanillic acid‐4‐sulfate (V4S), isovanillic acid‐3‐sulfate (IV3S) and benzoic acid‐4‐sulfate (B4S) and verified their purity (>98 %) using HPLC‐mass spectrometry. We tested the hypothesis that a mixture of these BB‐metabolites attenuates endothelial inflammation induced by lipotoxicity. Human aortic endothelial cells (HAEC) were treated ± BB‐metabolite mixture for 6 h and ± 500 μM palmitate for the last 5 h. The BB‐metabolite mixture contained V4S, IV3S, B4S, hydroxyhippuric acid, and hippuric acid at concentrations reported to peak in the blood 4 ‐ 6 h after consuming 240 g of blueberries in humans. Cell adhesion (assessed via human monocytic THP‐1 cells), and mRNA expression of ICAM‐1, VCAM‐1, E‐selectin, MCP1, IL‐8, NFκB‐p65, IKKβ, IKBα (assessed via qPCR), were quantified ± palmitate ± BB‐metabolites. Palmitate‐treatment increased (p<0.05) cell adhesion and increased (p<0.05) mRNA expression of ICAM‐1, VCAM‐1, E‐selectin, MCP‐1, IL‐8, and IKBα without affecting cell viability. All these effects were ameliorated (p<0.05) by BB‐metabolites. BB‐metabolites, at physiologically relevant concentrations suppressed lipotoxicity induced endothelial inflammation, which may be mediated via NFκB pathway. Blueberries might complement existing therapies to improve vascular complications.
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