Anti-allergic and anti-inflammatory properties of Zizyphus mauritiana root bark.

An allergy may sometimes be very dangerous and one of the main factors responsible for allergy is the complement system which can lead to a life-threatening reaction called anaphylaxis. Cycloxygenase-1 (COX-1), Cycloxygenase-2 (COX-2) and 5-Lipoxygenase (5-LOX) trigger allergic and inflammatory reactions. A number of anti-allergic synthetic drugs are available but are costly and show many side effects. Hence, the ancient traditional system of medication mentioned in Ayurveda finds an edge over various synthetic drugs. Zizyphus mauritiana is referred to as the store house of phytochemicals in Ayurveda. The stem and root barks of Zizyphus mauritiana were dried and powdered under controlled conditions. Extractions of the dried powders were performed separately in different solvents in increasing order of their polarity and were tested for their ability to inhibit the complement system. The aqueous extract of the root bark was found to be more effective in inhibiting the complement system. Fractionation of the aqueous extract resulted in the isolation of the Most Active Fraction (MAF) which inhibited the complement system, COX-1, COX-2, and 5-LOX with IC50 values of 0.006 µg ml(-1), 0.065 µg ml(-1), 0.008 µg ml(-1), and 0.083 µg ml(-1), respectively. The MAF was proven to be successful in down-regulating pro-inflammatory mediators like TNF-α, COX-2, and iNOS when tested on a RAW 264.7 cell line. In vivo, the MAF was found to be preventive against anaphylactic shock and the Arthus reaction, when orally administered daily to Wistar rats. Phytochemical analysis of the MAF has indicated that it is rich in tannins. Results indicate that the MAF, a fraction isolated from the aqueous extract of the root bark of Zizyphus mauritiana, has potent anti-allergic and anti-inflammatory properties.

Low-level laser therapy and sodium diclofenac in acute inflammatory response induced by skeletal muscle trauma: effects in muscle morphology and mRNA gene expression of inflammatory markers.

Pharmacological therapy is widely used in the treatment of muscle injuries. On the other hand, low-level laser therapy (LLLT) arises as a promising nonpharmacological treatment. The aim of this study was to analyze the effects of sodium diclofenac (topical application) and LLLT on morphological aspects and gene expression of biochemical inflammatory markers. We performed a single trauma in tibialis anterior muscle of rats. After 1 h, animals were treated with sodium diclofenac (11.6 mg g(-1) of solution) or LLLT (810 nm; continuous mode; 100 mW; 3.57 W cm(-2) ; 1, 3 or 9 J; 10, 30 or 90 s). Histological analysis and quantification of gene expression (real-time polymerase chain reaction-RT-PCR) of cyclooxygenase 1 and 2 (COX-1 and COX-2) and tumor necrosis factor-alpha (TNF-α) were performed at 6, 12 and 24 h after trauma. LLLT with all doses improved morphological aspects of muscle tissue, showing better results than injury and diclofenac groups. All LLLT doses also decreased (P < 0.05) COX-2 compared to injury group at all time points, and to diclofenac group at 24 h after trauma. In addition, LLLT decreased (P < 0.05) TNF-α compared both to injury and diclofenac groups at all time points. LLLT mainly with dose of 9 J is better than topical application of diclofenac in acute inflammation after muscle trauma.

Effects of low-level laser therapy (LLLT) and diclofenac (topical and intramuscular) as single and combined therapy in experimental model of controlled muscle strain in rats.

Muscle injuries represent ca 30% of sports injuries and excessive stretching of muscle causes more than 90% of injuries. Currently the most used treatments are nonsteroidal anti-inflammatory drugs (NSAIDs), however, in last years, low-level laser therapy (LLLT) is becoming an interesting therapeutic modality. The aim of this study was to evaluate the effect of single and combined therapies (LLLT, topical application of diclofenac and intramuscular diclofenac) on functional and biochemical aspects in an experimental model of controlled muscle strain in rats. Muscle strain was induced by overloading tibialis anterior muscle of rats. Injured groups received either no treatment, or a single treatment with topical or intramuscular diclofenac (TD and ID), or LLLT (3 J, 810 nm, 100 mW) 1 h after injury. Walking track analysis was the functional outcome and biochemical analyses included mRNA expression of COX-1 and COX-2 and blood levels of prostaglandin E2 (PGE2 ). All treatments significantly decreased COX-1 and COX-2 gene expression compared with injury group (P < 0.05). However, LLLT showed better effects than TD and ID regarding PGE2 levels and walking track analysis (P < 0.05). We can conclude that LLLT has more efficacy than topical and intramuscular diclofenac in treatment of muscle strain injury in acute stage.

Ethanol extract of Angelica gigas inhibits croton oil-induced inflammation by suppressing the cyclooxygenase - prostaglandin pathway.

The anti-inflammatory effects of an ethanol extract of Angelica gigas (EAG) were investigated in vitro and in vivo using croton oil-induced inflammation models. Croton oil (20 microg/mL) up-regulated mRNA expression of cyclooxygenase (COX)-I and COX-II in the macrophage cell line, RAW 264.7, resulting in the release of high concentrations of prostaglandin E(2) (PGE(2)). EAG (1 approximately 10 microg/mL) markedly suppressed croton oil-induced COX-II mRNA expression and PGE(2) production. Application of croton oil (5% in acetone) to mouse ears caused severe local erythema, edema and vascular leakage, which were significantly attenuated by oral pre-treatment with EAG (50 approximately 500 mg/kg). Croton oil dramatically increased blood levels of interleukin (IL)-6 and PGE(2) without affecting tumor-necrosis factor (TNF)-alpha and nitric oxide (NO) levels. EAG pre-treatment remarkably lowered IL-6 and PGE(2), but did not alter TNF-alpha or NO concentrations. These results indicate that EAG attenuates inflammatory responses in part by blocking the COX - PGE(2) pathway. Therefore, EAG could be a promising candidate for the treatment of inflammatory diseases.

The anti-inflammatory pharmacology of Pycnogenol in humans involves COX-2 and 5-LOX mRNA expression in leukocytes.

We investigated the effects of Pycnogenol supplementation on the arachidonic acid pathway in human polymorphonuclear leukocytes (PMNL) in response to an inflammatory stimulus. Pycnogenol is a standardised extract of French maritime pine bark consisting of procyanidins and polyphenolic monomers. Healthy volunteers aged 35 to 50 years were supplemented with 150 mg Pycnogenol a day for five days. Before and after the final day of supplementation, blood was drawn and PMNL were isolated. PMNL were primed with lipopolysaccharide (LPS) and stimulated with the receptor-mediated agonist formyl-methionyl-leucyl-phenylalanine (fMLP) to activate the arachidonic acid pathway and the biosynthesis of leukotrienes, thromboxane and prostaglandins. Pycnogenol supplementation inhibited 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) gene expression and phospholipase A2 (PLA2) activity. This effect was associated with a compensatory up-regulation of COX-1 gene expression. Interestingly, Pycnogenol suspended the interdependency between 5-LOX and 5-lipoxygenase activating protein (FLAP) expression. Pycnogenol supplementation reduced leukotriene production but did not leave prostaglandins unaltered, which we attribute to a decline of COX-2 activity in favour of COX-1. Here we show for the first time that Pycnogenol supplementation simultaneously inhibits COX-2 and 5-LOX gene expression and reduces leukotriene biosynthesis in human PMNL upon pro-inflammatory stimulation ex vivo.