Royal jelly for ulcerative colitis

Old Mike, if you are interested in this, one of the papers talks about its antioxidant effect as a possible mechanism, along with its immunological effects:

www.hindawi.com/journals/tswj/2015/956235/

article said...
Many aspects are involved in the inflammatory process, such as the oxygen reactive species (ROS), which have already been demonstrated to modulate the immune response. The respiration process is mandatory for the life of aerobic organisms, but it can be harmful due to the formation of ROS. Despite being considered foes, they play very important roles in living organisms. These molecules may exert an antibacterial function through protein, DNA, and lipid oxidation: on the other hand, when they are over produced, they become a threat to cells, due to their great oxidizing capacity [28]. There are extensive data showing that ROS are important players in the pathogenesis of IBD. Increased production of ROS harms the integrity of the epithelial cells, through an initial inflammatory response. In order to protect tissues against ROS-triggered injuries, all cells have antioxidant enzymes, including glutathione peroxidase (GSH-Px) and radical scavengers such as sulfhydryl compounds GSH [11].

GSH has already been shown to have its level diminished in experimental colitis [12]. This is part of the first line of defense against oxidative stress and the pretreatment with RJ 100 mg/kg was capable of increasing the levels of GSH (Table 2). These data suggest that RJ has the capacity of protecting intestinal mucosa from injuries, probably by protecting the depletion of this antioxidant barrier. These results are in accordance with previous studies showing that the RJ exerts a free radical scavenging activity [10], therefore ameliorating the ongoing inflammation.

Recent reports show that the cytosolic GSH-Px activity in rat colon tissues is altered in response to oxidative stress [29]. GSH-Px is an antioxidant enzyme that helps scavenging and inactivating H2O2, thereby protecting tissues from deleterious damage caused by the peroxide [30].

The activity of GSH-Px appeared reduced in TNBS-colitic groups (Table 2); this apparently paradox can be explained by the GSH and H2O2 dependence on the activity of the GSH-Px. For the TNBS group, the limiting factor is the level of GSH (very low); on the other hand, for the non-colitic saline group, the limiting factor is the H2O2, that is not augmented, since there is no oxidative stress going on. In both cases, The RJ 100 mg/kg was capable of increasing the level of GSH as well as the activity of GSH-Px, demonstrating its antioxidant property

And: www.ncbi.nlm.nih.gov/pmc/articles/PMC3167327/

article said...
Treatment of colitic rats with an oral dose of RJ gave a degree of recovery from acute colitis. The anti-colitogenic effects of RJ could be attributed to improvement of the antioxidant status of the animals due to an increase in mucin content of the colon mucosa.21 Polyphenolic compounds in their many forms are the main components responsible for the functional properties associated with many foods, such as antioxidant capacity22,23 and anti-inflammatory capacity.24 RJ contains polyphenolic compounds collected by bees from the plants where they gather nectar.25

Post Edited (xy123) : 7/19/2015 11:56:35 AM (GMT-6)

I'm planning to try them. Thanks pb4.

I read that Royal Jelly stimulates BH4 production and low BH4 production has been implicated in inflammation. The science does not seem agreed on though.

I use a honey that contains Royal Jelly, have not tried it alone. I remember circa 1980 someone suggesting that my Mum use it for MS, so it's interesting to see some more science around it now.

Looks like a biotech company is working on BH4
quartetmedicine.com/our-science/tetrahydrobiopterin-bh4-in-chronic-disease/
"Recent studies have also demonstrated that sulfasalazine and other structurally-related sulfa drugs are potent inhibitors of sepiapterin reductase (SPR), the final enzyme in the de novo synthesis pathway16-18. Sulfasalazine has been used clinically for over 60 years to treat autoimmune indications, such as ulcerative colitis and rheumatoid arthritis, despite a lack of understanding of the drug’s molecular mechanism of action. Linking the clinical activity of this approved drug to its modulation of BH4 synthesis provides an additional tie to human disease biology.

Safely restoring BH4 levels back to baseline by targeting one of the key BH4 synthetic enzymes has been shown to reduce inflammation and pain hypersensitivity in preclinical models7,15,19. Quartet is advancing its drug discovery efforts to develop small molecule therapies that can safely mimic the human genetic observations with pharmacological intervention"