Diabetic neuropathic pain (DNP) is associated with concurrent spinal cord autophagy activation, mTOR pathway activation, and neuroinflammation. However, the mechanistic interplay between these processes remains unclear, as mTOR activation typically suppresses autophagy under physiological conditions. This study investigates the role of spinal STING/ATG5-mediated autophagy in DNP pathogenesis and its relationship with mTOR signaling and neuroinflammatory pathways. Utilizing a rat model of DNP, we observed significant increases in spinal autophagosome density, LC3-II/LC3-I ratio, and STING/ATG5 expression, accompanied by elevated p-mTOR/mTOR ratios, compared to healthy controls. Notably, Beclin-1 expression remained unchanged. Pharmacological inhibition of STING or ATG5 silencing via intrathecal administration attenuated mechanical allodynia and reduced LC3-II/LC3-I ratios, whereas STING activation exacerbated pain behaviors while further upregulating STING/ATG5 expression and LC3-II/LC3-I ratios, but paradoxically decreased p-mTOR/mTOR ratios. mTOR inhibition with rapamycin alleviated DNP symptoms and suppressed TNF-α/IL-1β-mediated neuroinflammation, yet failed to modulate LC3-II/LC3-I ratios despite increasing Beclin-1 expression. Crucially, STING/ATG5 pathway manipulation did not alter pro-inflammatory cytokine levels, while rapamycin's analgesic effects correlated with anti-inflammatory activity. These findings demonstrate that STING/ATG5-driven autophagy contributes to DNP progression through a mechanism independent of both canonical mTOR-dependent autophagy regulation and inflammatory cytokine modulation. Conversely, mTOR inhibition exerts therapeutic effects predominantly via anti-inflammatory pathways rather than autophagy regulation. This study identifies a novel non-canonical autophagy pathway in DNP pathophysiology and clarifies distinct mechanistic bases for STING/ATG5-versus mTOR-targeted interventions.