Studies indicate that hyperglycemia-induced oxidative stress triggers the development of microvascular and macrovascular complications in diabetes. Accordingly, we hypothesized that maslinic acid (MA) prevents these complications due to its antioxidant properties. We, therefore, investigated the effects of 5-week MA treatment of streptozotocin (STZ)-induced diabetic rats on anti-oxidative status of cardiac, hepatic and renal tissues as well as on kidney function. Proximal tubular effects of MA were studied in anesthetized rats challenged with hypotonic saline after a 3.5 h equilibration for 4 h of 1 h control, 1.5 h treatment and 1.5 h recovery periods using lithium clearance. MA was added to the infusate during the treatment period. Oral glucose tolerance responses to MA were monitored in rats given a glucose load after an 18 h fast. Compared with untreated diabetic rats, MA-treated diabetic animals exhibited significantly low malondialdehyde (MDA, a marker of lipid peroxidation) and increased the activity of antioxidant enzymes; superoxide dismutase and glutathione peroxidase in hepatic, cardiac and renal tissues. The expressions of gastrocnemius muscle GLUT4 and kidney GLUT1 and GLUT2 were assessed to elucidate the mechanism of the hypoglycemic effects of MA. MA-treatment diminished the expression of GLUT1 and GLUT2 in diabetic kidney and reduced glycemia values of diabetic rats. MA administration increased urinary Na þ outputs and additionally the FE Na indicating that at least part of the overall reduction in Na þ reabsorption occurred in the proximal tubules. These results suggest antioxidant effects of MA can ameliorate oxidative stress and improve kidney function in diabetes mellitus.

Diabetes mellitus (DM) results from the inability of the pancreas to produce sufficient insulin or weakened cellular response to the insulin produced, which leads to hyperglycemia. Current treatments of DM focus on the use of oral hypoglycemic drugs such as acarbose, alpha-glucose inhibitors, sulphonylureas, thiazolidinediones, and biguanides to control blood glucose levels. However, these medications are known to have various side effects in addition to their bioavailability, efficacy, and safety concerns. These drawbacks have increased interest in the anti-diabetic potential of plant-derived bioactive compounds such as oleanolic and maslinic acids. Although their efficacy in ameliorating blood glucose levels has been reported in several studies, their bioavailability and efficacy remain of concern. The current review examines the anti-diabetic effects of oleanolic, maslinic, asiatic, ursolic, and corosolic acids and their derivatives, as well as the progress made thus far to enhance their bioavailability and efficacy. The literature for the current review was gathered from leading academic databases—including Google Scholar and PubMed—the key words listed below were used. The literature was searched as widely and comprehensively as possible without a defined range of dates.

Introduction: Reports indicate that oral administration of plant-derived maslinic acid (MA) exhibits hypoglycemic and renoprotective effects in streptozotocin (STZ)-induced diabetic rats. Challenges with triterpenes such as MA include low bioavailabilty which affects treatment efficacy in experimental animals. The goal of this study was to synthesize the MA derivative phenylhydrazine (PH-MA) in an effort to improve the efficacy of MA. Methods: Separate groups of non-diabetic and STZ-induced diabetic rats (n ¼ 6) were anesthetized and the jugular vein cannulated for the infusion of 0.077 M NaCl at 9 mL/h. The bladder was catheterized for collection the urine samples every 30 min. After 30.5 h equilibration period, consecutive 30 min urine collections were made over the subsequent 4 h of 1 h control, 1.5 h treatment, and 1.5 h recovery periods. PH-MA (22 mg/h) and MA (90 mg/h) were added during the treatment periods for analysis of proximal tubular Na þ handling, plasma aldosterone and arginine vasopressin in male Sprague-Dawley rats. Results: Intravenous infusion of PH-MA (22 mg/h) and MA (90 mg/h) significantly (p ˂ .05) increased Na þ output, fractional excretion of Na þ (FENa) and lithium (FELi). Interestingly, like MA, PH-MA significantly (p ˂ .05) increased glomerular filtration rate (GFR) over the treatment period and decreased plasma aldosterone levels. Our findings indicate that PH-MA inhibited sodium reabsorption in the proximal and distal tubule as shown by increased FENa and low plasma aldosterone levels, respectively. Conclusions: PH-MA is, therefore, a promising multitarget antidiabetic agent that may ameliorate kidney function of diabetic patients at a dose four times lower than the parent compound (MA).

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Malaria driven pathophysiology inimically conjoined to systemic inflammation response cascade in a vicious feed-forward cycle destined to a terrible debilitation or demise of the host. The Plasmodium parasite initiates physiological changes when it is transmitted into the human host by intermediate host and vector. Sporozoites injection elicits immunological and inflammatory response suppression facilitating movement into the blood stream undetected, destined to hepatocyte. Subsequently, hepatocyte invasion culminates in intracellular growth and conversion of the parasites rapturing hepatocytes releasing merozoites into the extrahepatic circulation. Inflammatory and immunological response initiation results in overt malarial disease symptoms. Initially, inflammatory response alleviates and curtails infection. Activation of leukocytes, lymphocytes, monocytes, and phagocytes secretes inflammatory mediators, chemokines, cytokines cytoadhering molecules which accelerate infection patency. Hormonal processes influence disease tolerance without necessarily interfering with parasitemia. Current treatment is anti-parasitic. Phytotherapeutic intervention in malaria is anti-parasitic and anti-disease effects that terminate the vicious cycle and alleviating disease. The phytochemicals, in malarial experimental and clinical work, include asiatic acid, maslinic acid, oleanolic acid, and inflammatory and immunological aberrations evolving in malaria and the effects of phytochemical therapeutics in the alleviation of the disease to enable leverage of future treatment regimens through harnessing existing plants materials is explored.

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Malarial systemic pathophysiology refers to physiological changes or abnormalities that are experienced by individuals infected with the Plasmodium parasite not be presenting in the absence of active, chronic or previous infection. The pathologies are derived, in part, from OS induced insults whose mediators are readily available in malaria. The malaria disease is equivalent to the pathophysiology as shown by the abnormal syndromic expressions ranging from ailments that affect homeostatic mechanisms and processes to tissues and organ specific damages and derangements. Phytotherapeutic remedies refer to the natural phytochemicals or plant medicinal compounds and their derivatives with known antiparasitic and antimalarial disease effects in both experimental and clinical situations. The chapter explores how Plasmodium infection generates or cause to be generated oxidative stress, how oxidative stress drives systemic disease process and how phytotherapeutics treatment (artemisinins) and administration (asiatic acid) in malaria resolves the various pathologies as a current situational analysis.