Plant-derived anti-inflammatory agents occupy an important position in natural product pharmacology because many compounds, extracts, and phytochemical classes interact with inflammatory mediators through distributed biological mechanisms rather than through a single isolated target. This article develops an original systems pharmacology framework for interpreting plant-derived anti-inflammatory evidence across agent identity, chemical characterization, target mapping, multi-target modulation, pathway crosstalk, oxidative stress interfaces, immune-metabolic context, safety evidence, and translational evidence boundaries. The framework is designed to distinguish plant-derived compounds, botanical extracts, and phytochemical classes from predicted targets, experimentally supported targets, inflammatory mediators, immune-cell contexts, pathway modulation, and clinical evidence. It emphasizes that multi-target modulation can support mechanistic hypothesis generation when target confidence, biological context, exposure plausibility, and validation needs are explicit. It also positions pathway crosstalk as a systems-level interpretive layer that requires causal caution because signaling changes do not automatically establish therapeutic benefit. Translational evidence mapping is proposed as a structured method for aligning in silico, in vitro, mechanistic, preclinical, safety, exposure, and human evidence with appropriate claim boundaries. The main contribution is a cautious, evidence-aware framework for organizing plant-derived anti-inflammatory research without presenting systems pharmacology, network inference, or biomarker modulation as clinical proof.