Does black cumin seed oil improve Crohn's symptoms?

Black Cumin (Nigella Sativa) Seed Oil from Wikipedia
"The oil contains melanthin, nigilline, damascenine and tannins. Melanthin is toxic in large doses and nigelline is paralytic, so this spice must be used in moderation."

"Effect of Black Cumin (Nigella Sativa)  Seed Oil on  Gastric Tissue in Experimental Colitis" in Advances in Environmental Biology (2011) [full text]
"The oil of NS is so beneficial due to its content of over 100 components such as aromatic oils, trace elements, vitamins and enzymes. It contains 58% of essential fatty acids including omega 6 and omega 3. These are necessary for the forming of prostaglandin E1 that balances and strengthens the immune system giving it the power to prevent infections and allergies and
control chronic illnesses.
...
Excessive production of pro-inflammatory mediators such as TNF-α, IL-1β, IL-6, IL-8, leukotriene B4 and platelet activating factor, and the presence of highly activated inflammatory cells such as neutrophils, monocytes and macrophages are common characteristic of ulcerative colitis [7,11,21]. Accordingly in the present study, serum TNF-α, IL-1β, and IL-6 increased in TNBS [trinitrobenzene sulphonic acid] induced colitis group. This inflammatory status has been reversed by NS [nigella sativa]oil.  Moreover increased serum LDH [lactate dehydrogenase] activity of the colitis group decreased with NS oil administration which shows the improved tissue damage by NS oil.
...
The use of natural anti-inflammatory products provides an attractive and relatively non-toxic alternative to modulate inflammatory disorders.  Consequently NS may have an important role in modulating the inflammatory response of the gastric tissue in colitis."

"Protective Effects of Nigella Sativa on Intestinal Ischemia-Reperfusion Injury in Rats" in Journal of Investigative Surgery (2010)

"Our results suggest that NS treatment protected the rat's intestinal tissue against intestinal ischemia- reperfusion injury."

"Rat Plasma Oxidation Status After Nigella Sativa L. Botanical Treatment in CCL4-Treated Rats" in
Toxicology Mechanisms and Methods (2008)
"The results indicate the potential of NS [nigella sativa] in preventing CCL4-induced toxic nitrosative stress. It is concluded that NS has marked antioxidant potentials that may be beneficial in alleviating complications of many illnesses related to oxidative/nitrosative stress in humans, but preclinical safety measures should be completed before clinical trials."

"Emerging clinical and therapeutic applications of Nigella sativa in gastroenterology" in World J Gastroenterol. (2009)

"N. sativa decreases DNA damage and thereby prevents initiation of carcinogenesis in colonic tissue secondary to exposure to toxic agents such as azoxymethane[2]. ... These anti-carcinogenic effects are mediated in part by thymoquinone secondary to its inhibitory influence on the NF-κB activation pathway[6].
... In fact, N. sativa attenuates the damage to β-cells of the pancreas following exposure to toxic elements such as cadmium[9]. Similarly, N. sativa administration attenuates the ulcerative effects of ethanol on gastric mucosa by decreasing the glutathione-S transferase levels in gastric mucosa[10].
Besides these effects, N. sativa also demonstrates anti- parasitic effects. For instance, its administration decreases the number of eggs as well as worms in schistosomiasis, which tends to affect hepatic and intestinal tissues[11]. In addition, N. sativa attenuates the side effects associated with some common medications used by gastroenterologists. For instance, cyclosporine, used by gastroenterologists for disorders such as recalcitrant Crohn’s disease, is often associated with nephrotoxic side effects, which can be limited by N. sativa due to its anti-oxidant properties[12]....
Thymoquinone, derived from N. sativa, has also been demonstrated to induce apoptosis of human colon cancer cells[15]. The above examples clearly illustrate the massive clinical and therapeutic potential of N. sativa. Personally, I believe that the anti-carcinogenic effects of N. sativa hold the maximum therapeutic potential. Given the significant benefits associated with its administration, broad-spectrum studies are clearly and urgently needed to further assess and elaborate its therapeutic benefits in gastroenterology."

Does flavonoid supplementation improve Crohn's symptoms?

Flavonoid from Wikipedia

Flavinoid mind map from Wikipedia (flavanols, flavones, anthocyanidines, isoflavonoids, neoflavonoids)

Formerly known as vitamin P

Flavonoids from the world's healthiest foods
"Flavonoids, an amazing array of over 6,000 different substances found in virtually all plants, are responsible for many of the plant colors that dazzle us with their brilliant shades of yellow, orange, and red.....While the flavonoid family is too complex to report all of its food connections, some highlights are especially important. In the fruit family, it is berries that come out highest in the chemical category of flavonoids called anthocyanins. Black raspberries, for example, may contain up to 100 milligrams of anthocyanins per ounce. ... In general the more colorful components of the food--like the skins of fruits--contain the highest concentration of flavonoids."

"Emerging Role of Antioxidants in the Protection of Uveitis Complications" in Current Medicinal Chemistry (2011)
"Many studies suggest that dark colored fruits such as berries; including blackberry, raspberry, and strawberry are rich in flavonoids and polyphenolic compounds and are endowed with beneficial properties in vision and eye health. ... All these antioxidants described here are well known to control the production of reactive oxygen species as well as their dependent activation of redox-sensitive transcription factors such as NF-κB and AP1. Further, most of the flavinoids have shown to prevent the activation of several key enymes [sic] such as aldose reductase that controls the oxidative stress signals."

Does increasing butyrates improve Crohn's symptoms?

Butyric acid from Wikipedia

"Butyrate Attenuates Lipopolysaccharide-Induced Inflammation in Intestinal Cells and Crohn's Mucosa through Modulation of Antioxidant Defense Machinery" in PLoS ONE (2012)
"Oxidative stress plays an important role in the pathogenesis of inflammatory bowel disease (IBD), including Crohn's disease (CrD). High levels of Reactive Oxygen Species (ROS) induce the activation of the redox-sensitive nuclear transcription factor kappa-B (NF-κB), which in turn triggers the inflammatory mediators. Butyrate decreases pro-inflammatory cytokine expression by the lamina propria mononuclear cells in CrD patients via inhibition of NF-κB activation, but how it reduces inflammation is still unclear. ... In conclusion, butyrate rescues the redox machinery and controls the intracellular ROS balance thus switching off EC-LPS induced inflammatory response in intestinal epithelial cells and in CrD colonic mucosa."

"Butyric Acid: an Ancient Controller of Metabolism, Inflammation and Stress Resistance" from Whole Health Source, Ancestral Nutrition and Health, Stephen Guyenet (2009)

See also my post entitled "Does butter improve Crohn's symptoms?"

What is the significance of reactive oxygen species (ROS) generation?

reactive oxygen species (ROS) generation from Wikipedia

"How This Normal Body Process Can Contribute to More Than 60 Diseases" from Mercola.com

"Mitochondrial reactive oxygen species drive proinflammatory cytokine production" in The Journal of Experimental Medicine (2011)
"High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn’s disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proinflammatory cytokine production. New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways."

"Autophagy Signaling Through Reactive Oxygen Species" in Antioxidants & Redox Signaling (2011)
"Autophagy is a degradative pathway that involves delivery of cytoplasmic components, including proteins, organelles, and invaded microbes to the lysosome for digestion. Autophagy is implicated in the pathology of various human diseases. The association of autophagy to inflammatory bowel diseases is consistent with recent discoveries of its role in immunity. A complex of signaling pathways control the induction of autophagy in different cellular contexts. Reactive oxygen species (ROS) are highly reactive oxygen free radicals or non-radical molecules that are generated by multiple mechanisms in cells, with the nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and mitochondria as major cellular sources. These ROS are important signaling molecules that regulate many signal-transduction pathways and play critical roles in cell survival, death, and immune defenses. ROS were recently shown to activate starvation-induced autophagy, antibacterial autophagy, and autophagic cell death. Current findings implicate ROS in the regulation of autophagy through distinct mechanisms, depending on cell types and stimulation conditions. Conversely, autophagy can also suppress ROS production. Understanding the mechanisms behind ROS-induced autophagy will provide significant therapeutic implications for related diseases."