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Animals were pretreated (1 hr beforestress) with saline (controls) or BPC 157 (dissolved insaline) (10 g or 10 ng/kg body wt intraperitoneallyor intragastrically) applied either alone to establishbasal conditions or, when manipulating the adrenergic or dopaminergic system, a simultaneousadministration was carried out with various agents withspecific effects on adrenergic or dopaminergic receptors[given in milligrams per kilogram intraperitoneally except for atenolol, which was givensubcutaneously] phentolamine (10.0), prazosin (0.5),yohimbine (5.0), clonidine (0.1) (-adrenergicdomain), propranolol (1.0), atenolol (20.0)(-adrenergic domain), domperidone (5.0), and haloperidol(5.0) (peripheral/central dopamine system).Alternatively, agents stimulating adrenergic ordopaminergic systemsadrenaline (5.0) or bromocriptine(10.0)-were applied

The inherent complexity, inter-individual variability, and dynamic nature of this axis necessitate further research to elucidate precise molecular mechanisms, validate therapeutic targets, and develop robust, clinically applicable biomarkers

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pneumoniae infection can release cytokines including TNF-, IL-1 and IL-6, which can affect the regulatory mechanisms of lipid metabolism and lead to lipid metabolism disorder such as elevation of plasma triglyceride and cholesterol levels (20)

In addition to the primary triggers of ferroptosis in OA (iron overload, mechanical overload, and inflammatory responses) discussed above, several other factors may further enhance ferroptosis in this context: (i) Elevated levels of ROS : These arise from mechanical stress, inflammatory responses and mitochondrial dysfunction, contribute significantly to ferroptosis by predisposing chondrocytes to oxidative damage, as these cells are particularly vulnerable to such stressors [126, 127, 128]