Frontiers in pharmacology · 2026
The inhibitory action of camel urine on human platelet surface glycoproteins could be the potential mechanism for its reported anticancer effects.
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Al-Ghumlas Abeer Khalid, Abdulla Maha Hamadien, El-Wetidy Mohammad S, Abdel Gader Abdel Gader Mohammad
Аннотация
BACKGROUND: Numerous medical properties have been attributed to camel urine (CU), including anticancer activity as reported in the literature. Laboratory studies have also demonstrated that CU inhibits platelet aggregation in a manner similar to aspirin (acetylsalicylic acid, ASP), a well-known antiplatelet agent with documented anticancer relevance. It is therefore of interest to further explore similarities in the actions of these agents using molecular approaches. This study aimed to characterize the effect of CU on the expression of human platelet GP receptors (CD41, CD61, CD42a, and CD42b) and to compare these effects with those of aspirin, a well-established antiplatelet agent.
METHODS: The effect of CU on human platelet aggregation in response to adenosine diphosphate (ADP) and arachidonic acid was evaluated using light transmission aggregometry. CU that showed an inhibitory effect on platelet aggregation was subsequently used for flow cytometric analysis, and ASP was used for comparison as a positive control. Platelet rich plasma was prepared from human blood, and washed platelets were subsequently isolated. The washed platelets were incubated with fresh CU (9.1% v/v; n = 8) or ASP (stock concentration: 81 mg/mL n = 6) for 5 min at room temperature, while parallel untreated samples served as controls. Platelet GP receptor expression was subsequently evaluated by flow cytometric quantification of CD61, CD41, CD42a, and CD42b using a BD FACSCalibur and BD FACSCanto II.
RESULTS: Flow cytometric analysis revealed that both CU and ASP caused a significant reduction in the expression of CD61, CD41, CD42a, CD42b, and the CD41/CD61 complex compared with untreated samples. However, ASP exhibited a stronger inhibitory effect than CU. ASP induced greater inhibition of CD41 (48.3%) followed by CD61 (41.5%), whereas CU resulted in 1: 30.6% and 28.2% inhibition of CD61 and CD41, respectively.
CONCLUSION: These findings indicate that CU possesses antiplatelet activity, which may warrant further investigation as a potential contributor to its reported anticancer effects.
METHODS: The effect of CU on human platelet aggregation in response to adenosine diphosphate (ADP) and arachidonic acid was evaluated using light transmission aggregometry. CU that showed an inhibitory effect on platelet aggregation was subsequently used for flow cytometric analysis, and ASP was used for comparison as a positive control. Platelet rich plasma was prepared from human blood, and washed platelets were subsequently isolated. The washed platelets were incubated with fresh CU (9.1% v/v; n = 8) or ASP (stock concentration: 81 mg/mL n = 6) for 5 min at room temperature, while parallel untreated samples served as controls. Platelet GP receptor expression was subsequently evaluated by flow cytometric quantification of CD61, CD41, CD42a, and CD42b using a BD FACSCalibur and BD FACSCanto II.
RESULTS: Flow cytometric analysis revealed that both CU and ASP caused a significant reduction in the expression of CD61, CD41, CD42a, CD42b, and the CD41/CD61 complex compared with untreated samples. However, ASP exhibited a stronger inhibitory effect than CU. ASP induced greater inhibition of CD41 (48.3%) followed by CD61 (41.5%), whereas CU resulted in 1: 30.6% and 28.2% inhibition of CD61 and CD41, respectively.
CONCLUSION: These findings indicate that CU possesses antiplatelet activity, which may warrant further investigation as a potential contributor to its reported anticancer effects.