Traditional oriental medicine for sensorineural hearing loss: Can ethnopharmacology contribute to potential drug discovery?

Phellodendri Cortex (Obaku in Japanese) and Coptidis Rhizoma (Oren), both of which contain berberine, have been used to prepare the kampo formula orengedokuto to treat inflammatory diseases, including dermatitis, gastric ulcers, and gastritis. These drugs are blended differently in other formulas, such as the use of Phellodendri Cortex in shichimotsukokato to treat hypertension and Coptidis Rhizoma in hangeshashinto to treat diarrhea and stomatitis. However, the differences in their medicinal properties are not well characterized. We prepared extracts from Phellodendron amurense bark (PAB) and Coptis chinensis rhizome (CCR) and separated them into alkaloid and non-alkaloid fractions. Anti-inflammatory effects were examined by monitoring the production of nitric oxide (NO), which is a pro-inflammatory mediator. A non-alkaloid fraction of the PAB extract suppressed NO production in hepatocytes more efficiently than that of the CCR extract. When each non-alkaloid fraction of the PAB and CCR extracts was administered to mice, the fractions of both extracts decreased the levels of mRNAs encoding inducible NO synthase and molecules in the interleukin-1β signaling pathway. Limonin and obakunone identified in the PAB non-alkaloid fraction suppressed NO production, exhibiting IC50 values of 16 and 2.6 μM, respectively, whereas berberine and coptisine displayed IC50 values of 12 and 14 μM, respectively. Limonin and obakunone reduced the expression of the iNOS gene, probably through the transcription factor nuclear factor-κB. Therefore, both limonoids and alkaloids may be responsible for the anti-inflammatory effects of the PAB extract, whereas alkaloids may be primarily responsible for those of the CCR extract. The different composition of the constituents may modulate the anti-inflammatory effects of Phellodendri Cortex and Coptidis Rhizoma.

Identification of anti-inflammatory constituents in Phellodendri Cortex and Coptidis Rhizoma by monitoring the suppression of nitric oxide production

Chronic kidney disease (CKD) is debilitating, increasing in incidence worldwide, and a financial and social burden on health systems. Kidney failure, the final stage of CKD, is life-threatening if untreated with kidney replacement therapies. Current therapies using commercially-available drugs, such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers and calcium channel blockers, generally only delay the progression of CKD. This review article focuses on effective alternative therapies to improve the prevention and treatment of CKD, using plants or plant extracts. Three mechanistic processes that are well-documented in CKD pathogenesis are inflammation, fibrosis, and oxidative stress. Many plants and their extracts are already known to ameliorate kidney dysfunction through antioxidant action, with subsequent benefits on inflammation and fibrosis. In vitro and in vivo experiments using plant-based therapies for pre-clinical research demonstrate some robust therapeutic benefits. In the CKD clinic, combination treatments of plant extracts with conventional therapies that are seen as relatively successful currently may confer additive or synergistic renoprotective effects. Therefore, the aim of recent research is to identify, rigorously test pre-clinically and clinically, and avoid any toxic outcomes to obtain optimal therapeutic benefit from medicinal plants. This review may prove to be a filtering tool to researchers into complementary and alternative medicines to find out the current trends of using plant-based therapies for the treatment of kidney diseases, including CKD. 

https://journals.sagepub.com/doi/pdf/10.1177/2515690X221079688

Promoting Plant-Based Therapies for Chronic Kidney Disease

Recent data highlight the role of the proximal tubule (PT) in reabsorbing, processing, and transcytosing urinary albumin from the glomerular filtrate Innovative techniques and approaches have provided exciting insights into these processes, and numerous investigators have shown that selective PT cell defects lead to significant albuminuria, even reaching nephrotic range in animal models Thus, the mechanisms of albumin reabsorption and transcytosis are undergoing intense study Working in concert with megalin and cubilin, a nonselective multireceptor complex that predominantly directs proteins for lysosomal degradation, the neonatal Fc receptor (FcRn) located at the brush border of the apical membrane has been implicated as the "receptor" mediating albumin transcytosis The FcRn pathway facilitates reabsorption and mediates transcytosis by its pH-dependent binding affinity in endosomal compartments This also allows for selective albumin sorting within the PT cell This reclamation pathway minimizes urinary losses and catabolism of albumin, thus prolonging its serum half-life It may also serve as a molecular sorter to preserve and reclaim normal albumin while allowing "altered" albumin to be catabolized via lysosomal pathways Here, we critically review the data supporting this novel mechanism

The proximal tubule and albuminuria: really!

Objective:Podocyte lesions lead to proteinuria and development of glomerulosclerosis in many renal diseases. However, podocyte lesions in patients with obesity-related glomerulopathy (ORG) and the underlying mechanisms remain unclear. In this study, we explored the relevance of podocyte lesions with renal damage and metabolic disturbance. Methodology:The absolute number of podocytes per glomerulus (Epi N/glom), the numerical density of podocytes per glomerulus [Nv(epi/glom)], and the mean glomerular volume were evaluated in 46 patients with ORG using the method of Weibel and Gomez (N=Nv×V, Nv=K/β√N3A/Vv). Renal tissue from the donors of kidney transplantation served as controls (n=10). The patients were further divided into two groups, according to with (Epi N/glom=337±77) or without (Epi N/glom=572±108) the decrease in the number of podocytes. Results:The glomerular volume increased and podocyte numerical density decreased (P0.001) in all of these patients. The glomerular volume [(4.69±0.99) vs (2.94±1.00)×10~6μm~3, P0.001] was significantly higher, while the podocyte density [(125±23) vs (203±39)×10~6μm~3, P0.001] was lower than that in controls. The endogenous creatinine clearance rate (Ccr) level [(134.66±24.57) vs (103.29±15.13)ml/(min·1.73m~2),P0.05] was markedly higher in patients without decrease of podocyte absolute number as compared to controls. However, proteinuria, the level of serum creatinine and the present of focal and segmental glomerularsclerosis (FSGS) (57.7% vs 75.0%, P=0.182) were relatively lower in ORG patients without podocyte reduction compared to those with reduction. In addition, a strong correlation was found between the absolute decrease in the number of podocyte and the present of hypertension (P=0.026), the impaired glucose tolerance (P=0.007), and the insulin resistance (P=0.044) in patients with ORG. The mean artery pressure (r=-0.639, P=0.002) and the level of cholesterol (r=-0.544, P=0.013) were inversely related to Epi N/glom only in the ORG patients with reduction of podocytes. Conclusion:A relative decrease of the density and an absolute decrease in the number of podocytes was observed in ORG patients, and varied at different stage of the disease. The descent in podocyte density was related to glomerular enlargement and capillary expanse, which might be reversible. However, the decrease of podocyte number was related to metabolism disorders and tended to FSGS, which suggested an irreversible lesion.

Podocyte lesions in patients with obesity-related glomerulopathy

Antihypertensive treatment is highly important to prevent the progression of chronic kidney disease. Shichimotsukokato (SKT), a traditional Japanese medicine (i.e., Kampo formula), lowered systolic blood pressure (SBP) in experimental animal models of hypertension. However, its mechanism of action has not been fully elucidated. We investigated the potential renoprotective mechanism of SKT in spontaneously hypertensive rats (SHRs). Ten-week-old SHRs were randomly divided into four groups (six rats per group). In the SHR control group, the SBP increased remarkably during the 8-week experimental period. In the SHRs, SKT extract administered orally at a daily dose of 0.45 or 0.15 g/kg significantly suppressed the increase in SBP to the same extent as telmisartan administered orally at a daily dose of 0.01 g/kg. At the end of the experiment, blood, urine, and kidney cortex tissue samples were examined. The SKT treatment significantly decreased urinary albumin excretion to nearly the same level as the telmisartan treatment. A notable loss of chloride channel 5 (ClC-5), a chloride channel in the proximal renal tubules, occurred in the SHR control group. Thus, we concluded that SKT administration significantly ameliorated this decrease. The mechanism of SKT in reducing urinary albumin excretion is mediated, at least partly, by prevention of the loss of ClC-5 in the renal cortex of SHRs.

The renoprotective effect of shichimotsukokato on hypertension-induced renal dysfunction in spontaneously hypertensive rats.

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The renoprotective effect of shichimotsukokato on hypertension-induced renal dysfunction in spontaneously hypertensive rats.