Trichinellosis is a global foodborne zoonotic disease. Numerous drugs used in its treatment exhibit inadequate absorption and diminished efficacy against encysted larvae in muscle tissue. Therefore, there is a need for innovative therapeutic agents to treat trichinellosis. Allium sativum (A. sativum), commonly known as garlic, is a bulbous plant that has been historically utilized in the treatment of various ailments. Currently, there is a paucity of data regarding the in vivo efficacy of A. sativum against trichinellosis. This study assessed the antiparasitic, anti-inflammatory, and antiapoptotic effects of A. sativum in murine models, independently or in conjunction with albendazole (ABZ), against the intestinal and muscular stages of trichinellosis. Fifty mice were equally categorized into five groups: negative control, positive control, ABZ, A. sativum, and a combination of ABZ and A. sativum. The effectiveness of the examined drugs was assessed through parasitological, biochemical, histological, and immunohistochemical methodologies. A. sativum resulted in a significant reduction of adult counts by 39.7% and larval counts by 54.4%. The inflammatory cellular infiltrate in the intestine and muscle was significantly reduced. In mice treated with A. sativum, serum levels of IFN-γ exhibited a significant increase, accompanied by a rise in Bcl-2 expression and a notable decrease in COX-2 expression. In conclusion, A. sativum demonstrates potential as a therapeutic agent for treating experimental trichinellosis, particularly during the muscle phase of the disease. It may serve as a safe promising therapy for trichinellosis.

Epidemiological studies indicate that Asian women have a lower incidence of breast cancer compared with their counterparts in the West, and soya consumption has been suggested as a contributory factor. Clinical and animal studies have revealed that cyclooxygenase-2 (COX-2) expression is associated with a risk of breast cancer. In the present study, we investigated the effect of soya isoflavones on the expression of COX-2 in the breast cell line MCF-7. Genistein, daidzein and equol were found to inhibit COX-2 expression induced by phorbol 12-myristate 13-acetate (PMA). Similar findings were observed in the COX-2 protein analysis. In order to study transcriptional control, a fragment of the 5′-flanking region of the hCOX-2 gene was amplified and inserted into a firefly luciferase reporter plasmid. The reporter assay indicated that the transactivation of the hCOX-2 promoter was induced by PMA, and activity was inhibited with the co-administration of genistein, daidzein or equol. An activator protein-1 (AP-1)/cyclic AMP response element binding protein (CREB) binding site (−59/−53) was identified in hCOX-2 promoter, and this could be critical in PMA-induced COX-2 expression. Truncation reporter plasmids with (−70/−36) and without (−51/−36) AP-1/CREB were constructed for subsequent analysis. The results revealed that the hCOX-2 promoter transactivation suppressed by isoflavone could be dependent on AP-1/CREB binding. Nonetheless, this study illustrated that the soya isoflavones reduced COX-2 expression, which could be important in the post-initiation events of breast carcinogenesis.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of arthritis and pain. However, their long-term use is limited by gastrointestinal (GI) side effects such as gastric ulcers. NSAIDs act by inhibiting an enzyme called cyclooxygenase. Cyclooxygenase (COX) catalyses the generation of prostaglandins from arachidonic acid. Two isoforms of the enzyme exist – COX-1 and COX-2 – both of which are targets for NSAIDs. Although they are associated with GI toxicity, NSAIDs have important antithrombotic and anti-inflammatory effects. The GI injury has been attributed to COX-1 inhibition and the anti-inflammatory effects to COX-2 inhibition. As COX-2 is traditionally viewed as an inducible enzyme, selective inhibition of COX-2 by ‘coxibs’ (selective COX-2 inhibitors) has been employed to achieve anti-inflammatory and analgesic effects without GI side effects. However, recently there have been suggestions that chronic administration of coxibs might increase the risk of cardiovascular events, such as atherosclerosis, compared with traditional NSAIDs. In vascular disease, there is increased expression of both COX-1 and COX-2, resulting in enhanced prostaglandin generation. The specific role of COX-1 and COX-2 in vascular regulation is still unknown but such knowledge is essential for the effective use of coxibs. Although more evidence is pointing to selective COX-1 inhibition as a therapeutic measure in inflammatory atherosclerosis, there are some studies that suggest that inhibition of COX-2 might have a potential benefit on atherosclerosis.