Figure 4.

Protective mechanisms of M. oleifera against kidney injury. M. oleifera increased the production of catalase (CAT); superoxide dismutase (SOD); glutathione peroxidase (GPx); glutathione (GSH); total antioxidant capacity (TAC); delta-amino levulinic acid dehydratase (ALAD); and G-6-Pase, which facilitated oxidative stress reduction by activating glutathione (GSH), a non-protein thiol that suppresses free radicals. GSH suppresses the oxidative stress situation. M. oleifera also suppressed oxidative stressors caused by ROS, H₂O₂, GSSG, and LPO by inhibiting MDA, LPP, TPCC, BUN, Creatinine, and NO. Bcl-2 was similarly produced by stress stimuli and was linked to the suppression of necrosis, induced by M. oleifera. M. oleifera inhibited the expression of Caspase-9, a protein involved in the formation of caspases. Following NF-kB, stress stimuli also increased CRP expression. NF-kB then moved from the cytosol to the nucleus, bound to DNA, and activated inflammation-related proteins. M. oleifera inhibited the mechanism by which inflammation factors were produced, hence, reducing inflammation. M. oleifera has been linked to a reduction in the progression of kidney disease.