@article {1258, title = {Camel Milk Supplemented with Fenugreek Seeds Improve Lipid Profile, Atherogenic Index and Antioxidative Status in Animal Model of Cardiovascular Disorders}, journal = {Pharmacognosy Research}, volume = {16}, year = {2024}, month = {June 2024}, pages = {483-489}, type = {Original Article}, chapter = {483}, abstract = {

Background: Despite of advancement in the technology and an improvement in handing of patients with atherosclerosis and Cardiovascular Diseases (CVDs) but the mortality associated with them remains to be highest in all over the globe. The Atherogenic Index of Plasma (AIP) has now been considered to be a best indicator for the analysis of atherosclerosis and CVDs. This study was undertaken to investigate the potential of Fermented camel Milk (FM) and Fenugreek seed powder (FG) on the animal model of CVDs. Materials and Methods: The animal models of atherosclerosis and CVDs were made by feeding of rats with high fat and cholesterol diets and the effect of FM supplemented with FG either alone or in a combination (FGFM) were tested on the lipid profile and AIP by Total Antioxidant Capacity (TAC), Malondialdehyde (MDA), Glutathione Peroxidase (GPx) activity, Total Cholesterol (TC) and small dense Low-Density Lipoprotein (sd-LDL). Results: The data revealed that FM, FG and their combination potentially increased in TAC level (p\<0.05) and decreased in lipid peroxidation via reduction in the serum concentrations of MDA. Whereas, experimental rats on FM were fully restored GPx activity. Moreover, FM and FG and their combination lowered TC and sd-LDL concentrations significantly (p\<0.05). Conclusion: The novel findings of this study clearly indicated that the FG, FM and FGFM have potential in preventing the onset of atherosclerosis and CVDs by reducing the levels of sd-LDL and improving lipids profile, AIP and antioxidant capacity.

}, keywords = {Camel milk, Cardiovascular disorders, Fenugreek, High fat diet, Lipid profile}, doi = {10.5530/pres.16.3.58}, author = {Sami A. Althwab and Thekra A. Alharby and Waleed Al Abdulmonem and Khalid H. Musa and Zafar Rasheed and Abdullah S. M. Aljohani and Mona S. Almujaydil and Bashayr Y. Alghonaim and Nasser A. Alharbi and Ala Al Rajabi and Muhammad Ismail Khan and Nelson Fern{\'a}ndez and Essam M. Hamad} } @article {490, title = {Lactoferrin from Camelus dromedarius Inhibits Nuclear Transcription Factor-kappa B Activation, Cyclooxygenase-2 Expression and Prostaglandin E2 Production in Stimulated Human Chondrocytes}, journal = {Pharmacognosy Research}, volume = {8}, year = {2016}, month = {February 2016}, pages = {135-141}, type = {Original Article}, chapter = {135}, abstract = {

Background: Osteoarthritis (OA) is a progressive joint disorder, which remains the leading cause of chronic disability in aged people. Nuclear factor-kappa B (NF)-κB is a major cellular event in OA and its activation by interleukin-1β (IL-1β) plays a critical role in cartilage breakdown in these patients. Objective: In this study, we examined the effect of lactoferrin on NF-κB activation, cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) production in stimulated human articular chondrocytes. Materials and Methods: Human chondrocytes were derived from OA articular cartilage and treated with camel lactoferrin and then stimulated with IL-1β. Gene expression was determined by TaqMan assays and protein expression was studied by Western immunoblotting. NF-κB activity and PGE2 levels were determined by ELISA based assays. NF-κB activity was also determined by treatment of chondrocytes with NF-κB specific inhibitor Bay 11{\textendash}7082. Results: Lactoferrin inhibited IL-1β-induced activation and nuclear translocation of NF-κB p65 in human OA chondrocytes. Lactoferrin also inhibited mRNA/protein expression of COX-2 and production of PGE2. Moreover, Bay 11{\textendash}7082 also inhibited IL-1β-induced expression of COX-2 and production of PGE2. The inhibitory effect of lactoferrin on the IL-1β induced expression of COX-2 or production of PGE2 was mediated at least in part via suppression of NF-κB activation. Conclusions: Our data determine camel lactoferrin as a novel inhibitor of IL-1β-induced activation of NF-κB signaling events and production of cartilage-degrading molecule PGE2 via inhibition of COX-2 expressions. These results may have important implications for the development of novel therapeutic strategies for the prevention/treatment of OA and other degenerative/inflammatory diseases.

}, keywords = {Chondrocytes, Cyclooxygenase-2, interleukin-1β, lactoferrin, nuclear factor-kappa B, osteoarthritis, Prostaglandin E2}, doi = {10.4103/0974-8490.175612}, author = {Naila Rasheed and Abdullah Alghasham and Zafar Rasheed} }