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Effects of morroniside isolated from Corni Fructus on renal lipids and inflammation in type 2 diabetic mice
Chan Hum Park1, Jeong Sook Noh, Takashi Tanaka
1Institute of Natural Medicine, University of Toyama, Toyama, Japan.
Objectives:
The effects of morroniside isolated from Corni Fructus on renal lipids and inflammation provoked by hyperglycaemia were investigated using type 2 diabetic mice.
Methods:
Morroniside was administered orally to db/db mice at 20 or 100 mg/kg daily for 8 weeks, and its effects were compared with those in vehicle-treated db/db and m/m (non-diabetic) mice. Serum and renal biochemical factors and protein expression related to lipid homeostasis and inflammation were measured.
Key Findings:
Morroniside produced significant dose-dependent reductions in serum triglyceride and renal glucose and lipid levels. Morroniside altered the abnormal protein expression of sterol regulatory element binding proteins (SREBP-1 and SREBP-2). In addition, the formation of reactive oxygen species and lipid peroxidation were inhibited in the morroniside-treated db/db mouse group, and the ratio of reduced glutathione to the oxidised form was significantly elevated. These results suggest that morroniside alleviated oxidative stress in the kidneys of db/db mice. Furthermore, 100 mg/kg morroniside down-regulated the expression of nuclear factor-kappaBp65, cyclooxygenase-2 and inducible nitric oxide synthase augmented in db/db mice.
Conclusions:
Morroniside may inhibit abnormal lipid metabolism and inflammation due to reactive oxygen species in the kidneys in type 2 diabetes.
Insights
Morroniside, derived from Corni Fructus, effectively reduced kidney lipids and inflammation in type 2 diabetic mice. This natural compound shows promise for managing diabetic nephropathy by improving lipid metabolism and alleviating oxidative stress.
Area of Science:
- Pharmacology
- Nephrology
- Metabolic Diseases
Background:
- Hyperglycemia in type 2 diabetes mellitus (T2DM) leads to significant renal complications, including abnormal lipid metabolism and inflammation.
- Diabetic nephropathy is a major cause of end-stage renal disease, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the therapeutic effects of morroniside, a compound isolated from Corni Fructus, on renal lipid accumulation and inflammation in a mouse model of T2DM.
- To elucidate the underlying mechanisms by which morroniside impacts lipid homeostasis and oxidative stress in the diabetic kidney.
Main Methods:
- Administration of morroniside (20 or 100 mg/kg/day) orally to db/db mice (T2DM model) for 8 weeks.
- Comparison with vehicle-treated db/db mice and non-diabetic m/m mice.
- Assessment of serum and renal biochemical parameters, including lipids and glucose.
- Measurement of protein expression related to lipid metabolism (SREBP-1, SREBP-2) and inflammation (NF-κB, COX-2, iNOS).
- Evaluation of oxidative stress markers, including reactive oxygen species (ROS), lipid peroxidation, and glutathione levels.
Main Results:
- Morroniside treatment resulted in significant, dose-dependent reductions in serum triglyceride and renal glucose and lipid levels.
- The compound normalized the expression of sterol regulatory element-binding proteins (SREBP-1 and SREBP-2), indicating improved lipid homeostasis.
- Morroniside inhibited the formation of reactive oxygen species and lipid peroxidation while increasing the ratio of reduced to oxidized glutathione, suggesting alleviation of oxidative stress.
- Down-regulation of key inflammatory markers, including nuclear factor-kappa B p65 (NF-κB p65), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), was observed at the higher dose.
Conclusions:
- Morroniside demonstrates significant potential in ameliorating abnormal lipid metabolism and inflammation in the kidneys of type 2 diabetic mice.
- The protective effects are likely mediated through the inhibition of oxidative stress and inflammatory pathways.
- Corni Fructus-derived morroniside represents a promising natural compound for managing diabetic kidney disease.
