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As illustrated in Figure 3, pro-inflammatory cytokines, including TNF-, IL-1, and IL-6, promote OA progression by activating signaling intermediates such as p38 and ERK1/2, leading to upregulation of matrix metalloproteinases (MMPs) and degradation of cartilage structure

Those cellular components are returned to the patient with FFP or albumin

Hence, the interaction of the antibiotics with the plasma membrane of mammalian cells is limited in comparison with that of bacterial membranes [38]