Assessing the Effectiveness of Panchatikta Ghrita, a Classical Ayurvedic Formulation as Add-on Therapy to Vitamin D3 and Calcium Supplements in Patients with Osteopenia: A Randomized, Open-Labeled, Comparative, Controlled Clinical Study.

Objectives: To assess the change in the bone mineral density (BMD) score, bone-specific biomarkers (serum vitamin D3, tartrate-resistant acid phosphatase 5b [TRAP-5b], and osteocalcin), quality of life, Ayurvedic symptoms (Asthikshaya Lakshanas), and fracture risk assessment tool (FRAX) scores following treatment with Panchatikta Ghrita (PG), a classical herbal formulation as add-on therapy to calcium and vitamin D3 supplements. Study design: Randomized, open-labeled, comparative, controlled clinical study. Location: TN Medical College and BYL Nair Hospital, Mumbai, India. Study participants: Eighty adult patients, aged between 40 and 75 years, diagnosed to have osteopenia (BMD T-score between -1 and -2.5 in at least two of the three joints tested-lumbar spine L1-L4, left femur-neck, left forearm-radius total). Study intervention: Treatment group received two tablespoons of PG (10 mL in lukewarm milk) along with calcium and vitamin D3 supplements twice a day, whereas control group received only calcium and vitamin D3 supplements twice a day for a period of 12 months. Outcome measures: BMD, bone-specific biomarkers (vitamin D3, TRAP-5b, and osteocalcin), quality of life, Ayurvedic symptoms, and FRAX scores were evaluated before and at 6 and 12 months. Results: Eighty patients were enrolled; of which, 65 patients completed the study while 15 patients dropped out. Improvement in the BMD scores was observed at 6 and 12 months with the maximum benefit in the lumbar spine region. Significant improvement in the bone-specific biomarkers, namely serum vitamin D3 (p < 0.001), osteocalcin (p < 0.001), and TRAP-5b (p < 0.05), was observed in the PG-treated group compared with the standard treatment group. Improvement in the quality of life, Ayurvedic symptoms scores, and risk reduction in FRAX scores of major osteoporotic fracture risk and hip fracture risk was greater with PG, although not statistically significant. Conclusions: The study findings demonstrate that PG slows down the bone degeneration processes by its stabilizing effect on the bone-specific biomarkers, indicating its potential usefulness as preventive therapy in osteopenia. The positive improvement noted in this study needs to be confirmed in studies with a larger sample size and longer duration.

Chrysin ameliorates nonalcoholic fatty liver disease in rats.

Nonalcoholic fatty liver disease (NAFLD) is regarded as the hepatic manifestation of the metabolic syndrome. It begins with the accumulation of fat in the liver (simple steatosis), which if untreated can progress to nonalcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma. Chrysin is a flavonoid present in bee propolis and many other plants. The objective of this study was to determine if chrysin can ameliorate NAFLD induced by feeding a high fructose diet (HFD) in rats. The rats were divided into five groups: normal control, HFD control, chrysin (25, 50, and 100 mg/kg p.o. body weight). Biochemical estimations were carried out in the serum and liver of rats. The gene expressions of SREBP-1c and PPAR α were determined in the liver. The histopathology of the liver was also studied. Chrysin caused a significant decrease in the serum fasting glucose and improved the insulin resistance, dyslipidemia, and liver enzymes. It caused a significant decrease in the liver weight and hepatic free fatty acids, triglyceride, and cholesterol content. Chrysin exerted antioxidant effects, reduced carbonyl content, advanced glycation end products, collagen, TNF-α, and IL-6 concentrations in the liver. Chrysin significantly reduced the hepatic gene expression of SREBP-1c and increased that of PPAR-α. The histopathology of liver of rats treated with chrysin showed significant decrease in the steatosis, ballooning, and lobular inflammation when compared to the HFD control group. Thus, chrysin demonstrated anti-steatotic, antiglycating, antioxidant, anti-inflammatory, and antifibrotic effects and seems to be a promising molecule for the management of NAFLD.

Plumbagin reduces obesity and nonalcoholic fatty liver disease induced by fructose in rats through regulation of lipid metabolism, inflammation and oxidative stress.

BACKGROUND: Chronic consumption of fructose causes obesity and nonalcoholic fatty liver disease (NAFLD). Currently available therapies have limitations; hence there is a need to screen new molecules. Plumbagin is a naphthoquinone present in the roots of Plumbago species which has hypolipidemic and hepatoprotective activities. METHODS: Rats were divided into five groups: normal control, disease control, orlistat, plumbagin (0.5 mg/kg and 1 mg/kg body weight). The normal control group received standard diet and drinking water while the remaining groups received fructose in drinking water alongwith the standard diet for 16 weeks. Orlistat and plumbagin were administered orally from the 9th week-16th week. The body weight, calorie intake and weights of visceral adipose tissue and liver were determined. Blood glucose, insulin, lipid profile and liver function tests were determined. Antioxidant and inflammatory parameters, lipids and collagen were determined in the liver. Gene expression of SREBP-1c and PPAR-α were determined in the liver. The histopathology of the adipose tissue and liver were also studied. RESULTS: Fructose feeding resulted in a significant increase in the body weight gain, calorie intake, visceral fat, liver weight, blood glucose and insulin and caused dyslipidemia which was mitigated by plumbagin. Plumbagin exerted antioxidant, anti-inflammatory and anti-fibrotic effects in the liver and reduced the hepatic lipids. Plumbagin reduced the gene expression of SREBP-1c and increased that of PPAR-α. Plumbagin reduced the hypertrophy of adipocytes and ameliorated the degenerative changes in the liver. CONCLUSION: Plumbagin thus seems to be a promising molecule for the management of obesity and NAFLD.

Alterations in Lipid Metabolism and Antioxidant Status in Lichen Planus.

BACKGROUND: Lichen planus (LP), a T-cell-mediated inflammatory disorder, wherein inflammation produces lipid metabolism disturbances, is linked to increase in cardiovascular (CV) risk with dyslipidemia. Increased reactive oxygen species and lipid peroxides have also been implicated in its pathogenesis. AIM AND OBJECTIVE: The aim of the study was to evaluate the status on lipid disturbances, oxidative stress, and inflammation in LP patients. MATERIALS AND METHODS: The study was initiated after obtaining Institutional Ethics Committee permission and written informed consent from participants. The study included 125 patients (74 LP patients and 51 age and sex-matched controls) visiting the outpatient clinic in the dermatology department of our hospital. Variables analyzed included lipid profile, C-reactive protein (CRP), malondialdehyde (MDA), and catalase (CAT) activity. RESULTS: Analysis of lipid parameters revealed significantly higher levels of total cholesterol (TC), triglycerides, and low-density lipoprotein cholesterol (LDL-C) along with decreased levels of high-density lipoprotein cholesterol (HDL-C) in LP patients as compared to their respective controls. LP patients also presented with a significantly higher atherogenic index that is, (TC/HDL-C) and LDL-C/HDL-C ratios than the controls. A significant increase in CRP levels was observed among the LP patients. There was a statistically significant increase in the serum levels of the lipid peroxidation product, MDA and a statistically significant decrease in CAT activity in LP patients as compared to their respective controls. A statistically significant positive correlation (r = 0.96) was observed between serum MDA levels and duration of LP whereas a significantly negative correlation (r = -0.76) was seen between CAT activity and LP duration. CONCLUSION: Chronic inflammation in patients with LP may explain the association with dyslipidemia and CV risk. Our findings also suggest that an increase in oxidative stress and imbalance in the antioxidant defense mechanisms in LP may play a role in the pathogenesis of LP.