Ginger (Zingiber officinale Roscoe, Zingiberaceae), a commonly used botanical inthe United States, is primarily known for
Its anti-emetic properties. However, it has also been used medicinally since antiquity as an anti-inflammatory. In modern usage, particular attention has focused on the cyclooxygenase (COX)-inhibiting effects of the gingerols, phenolic compounds that are responsible for ginger’s pungent taste, and their potential use in treating inflammatory disorders such as arthritis. Previously, we demonstrated potent anti-arthritic effects of gingerol-containing extracts of ginger in an experimental model of rheumatoid arthritis (RA). However, crude extracts containing both of ginger’s secondary metabolites, the gingerols and the essential oils, were even more potent in inhibiting joint swelling than gingerols alone. Having previously demonstrated
anti-arthritic effects of both the phenolic and essential oil fractions of turmeric (Curcuma longa L., Zingiberaceae), a plant that is botanically and chemically related to ginger, we postulated that the essential oils of ginger could similarly be bioactive with
respect to inhibition of joint inflammation and thus contribute to ginger’s potential anti-arthritic effects.
To test this postulate, studies were undertaken to examine the Joint protective effects of the isolated essential oils of
ginger (GEO), secondary metabolites that are responsible for ginger’s characteristic aroma. For these studies, the streptococcal cell wall (SCW)-induced arthritis model of RA previously employed by our laboratory to test other ginger (and turmeric) extracts was employed to facilitate comparisons with chemically-related extracts. In this model, the inflammatory reaction in response to streptococcal cell wall(SCW) deposition within joints recapitulates the histopathology of RA; female Lewis rats develop an initial, transient phase of joint swelling that is characterized by an influx of neutrophils and other inflammatory cells (acute phase, days 0–5), followed by a recrudescence of joint swelling that is
associated with synovial hyperplasia and progressive destruction of periarticular bone by the invading synovium (chronic phase,
days 10–28). Additionally, classic granulomas form within the liver at sites of hepatic SCW deposition, an inflammatory response that can be protective in certain settings, such as pulmonary tuberculosis where invading bacilli are walled off within granulomas, thus helping to quell the spread of infection.
In our previous studies, SCW-induced arthritis and granulomatous inflammation were each more effectively blocked by a
Crude ginger extract containing GEO and gingerols as compared to a gingerol-only fraction. The crude extract almost completely prevented both phases of joint swelling (93% and 97% inhibition of acute and chronic arthritis, respectively), while the gingerol-only fraction was less effective (78% and 62% inhibition, respectively). The crude extract also blocked granulomatous inflammation by 76%, while the gingerol-only fraction was without effect. Therefore, effects of isolated GEO on joint inflammation and the granulomatous hepatic response were tested here using the SCW model. In addition, because estrogenic effects have been reported in vitro for certain monoterpenes present in GEO, in vivo treatment effects of GEO in the SCW model were compared to those of 17-b estradiol (E ). While joint protective effects of estrogen have previously been reported inpre-clinical RA models and have been postulated for RA itself due to the clinical observation of improved disease activity during pregnancy, effects of estrogen in the SCW-model in female rats have, to our knowledge, not previously been reported.