Aframomum genus represents an enormous resource for novel compounds with a range of medicinal properties. However, these plants are under-researched and their conservation is poor. To unravel their full potential, efforts should be strengthened throughout the continent to establish the taxonomy, preserve the genus and explore novel medicinal properties.

Objective: To evaluate the scientific basis for the use of Kang 601 heji (K-601) as an anti-inflammatory and antipyretic agent using appropriate animal models. Methods: Carrageenan-induced rat paw and xylene-induced ear oedemas were models used to investigate anti-inflammatory actions of K-601. Lipopolysaccharide-induced pyrexia model was used to evaluate antipyretic activity in Wistar rats. The antiinflammatory and antipyretic mechanisms were evaluated by detecting prostaglandins E 2 , nitric oxide, interleukin-1b and tumour necrosis factor-a levels using appropriate reagents and ELISA kits. Results: The results revealed that K-601 reduced the level of inflammations in both antiinflammatory models in a dose-dependent manner. The same was true for the antipyretic model. The possible mechanisms of actions were through the inhibition of prostaglandins E 2 , interleukin-1b, tumour necrosis factor-a and nitric oxide. Conclusions: K-601 has proven anti-inflammatory and antipyretic actions. The findings provide a scientific basis for the use of K-601 as anti-inflammatory and antipyretic agent in traditional Chinese medicinal practice.

1-[4-[2-(4-Bromobenzene-sulfonamino)ethyl]phenylsulfonyl]-3-(trans-4-methylcyclohexyl) urea (G004, CAS865483-06-3) is a synthetic sulfonylurea, incorporating the hypoglycemic active structure of glimepiride (CAS 93479-97-1) and anti-TXA2 receptor (TP) active structure of BM-531(CAS 284464-46-6). In this study, we evaluated the effect of G004 on hyperglycemia and dyslipidemia as well as diabetic nephropathy (DN) in db/db mice by gavage over 90 consecutive days of treatment. The fasting blood glucose (FBG), glucose, and insulin tolerance as well as dyslipidemia were effectively ameliorated in db/db mice treated with G004. Interestingly, renal histological results of db/db mice revealed that G004 markedly reversed the expansion of mesangial extracellular matrix (ECM), the early hallmark of DN. Indeed, G004 treatment downregulated the renal expressions of type 4 collagen (Col IV) and transforming growth factor-β1 (TGF-β1) in db/db mice. In addition, imbalance in expressions of matrix metalloproteinase-9 (MMP-9) and its tissue inhibitor-1 (TIMP-1) in db/db mice kidneys was observed. However, G004 increased and decreased the expressions of MMP-9 and TIMP-1, respectively. It is well known that TGF-β pathway signaling plays an essential role in hyperglycemia-induced cell protein synthesis. On the other hand, MMP/TIMP system is responsible for the breakdown and turnover of ECM. Thus, we speculate that G004 possibly attenuated ECM accumulation via remodeling the synthesis and degradation of ECM component Col IV through modulation in TGF-β1 and MMP-9/TIMP-1 expressions in kidneys of db/db mice. Results from this study provide a strong rationale for G004 to be an efficient glucose-controlling agent with significant reno-protective properties.