Coir pith, an agro-industrial residue, is resistant to natural degradation, and its accumulation causes environmental pollution. Ferulic acid, a precursor of vanillin, was extracted from the raw coir pith by chemical pre-treatment such as alkaline hydrolysis, acidification, and liquid–liquid extraction method. The obtained ferulic acid (1.2 g/50 g) was analysed using high-performance liquid chromatography (HPLC) and used as a substrate for biotransformation by Aspergillus niger to vanillic acid, which, in turn, was fermented by using Phanerochaete chrysosporium to vanillin. The quantity of vanillic acid detected by HPLC on the third day of incubation was 0.773 g/L, while the optimal yield of vanillin on the subsequent third day of incubation was 0.628 g/L. Thus, the chemical extraction of ferulic acid from coir pith ensued bioconversion into vanillin. These products are highly valuable and economical to be used in industries such as pharmaceuticals, health, cosmetics, and neutraceuticals. Graphical Abstract

In cervical cancer chemotherapy, paclitaxel (PTX) chemoresistance has become a major difficulty, and it also affects the survival rate of numerous tumor patients. Thus, for the reversal of chemoresistance, it is imperative to develop combinatory drugs with petite or almost no side effects to sensitize cells to paclitaxel. Ginsenoside Rg5 (GRg5) may act as a chemosensitizer by reversing multidrug resistance. The present study aimed to determine the potential of GRg5 as a chemosensitizer in PTX-resistant human cervical adeno-carcinoma cell lines (HeLa cells). MTT assay was carried out to assess whether GRg5 can potentiate the cytotoxic effect of PTX in PTX- resistant HeLa cells; using flow cytometry-based annexin V-FITC assay, cellular apoptosis was analyzed; the rate of expression of the cell cycle, apoptosis and major cell-survival-signaling-related genes and its proteins were examined using RT-PCR and Western blotting technique. We found increased mRNA expression of Bak, Bax, Bid, and PUMA genes, whereas the mRNA expression of Bcl2, Bcl-XL, c-IAP-1, and MCL-1 were low; GRg5 combination triggered the efficacy of paclitaxel, which led to increased expression of Bax with an enhanced caspase-9/-3 activation, and apoptosis. Moreover, the study supports GRg5 as an inhibitor of two key signaling proteins, Akt and NF-κB, by which GRg5 augments the susceptibility of cervical cancer cells to PTX chemotherapy. GRg5 drastically potentiated the antiproliferative and pro-apoptotic activity of paclitaxel in PTX-resistant human cervical cancer cells in a synergistic mode. Moreover, in the clinical context, combining paclitaxel with GRg5 may prove to be a new approach for enhancing the efficacy of the paclitaxel.

Pituitary gonadotropins directly govern ovarian functions, which are in turn regulated by the ovarian steroid hormones. The precise interplay of gonadotropins and steroid hormones is critical for follicle growth and differentiation. Furthermore, autophagy regulates ovarian follicle differentiation. However, how the high-fat-high fructose (HFD-HF) diet regulates gonadotropins and facilitates autophagy-mediated follicular differentiation in the ovary is obscure. We fed prepubertal rats (PND 25) an HFD-HF diet until PND 90. The results showed diminished adenohypophyseal GnRHR, PR, and aromatase expression, whereas AR, ERα, PRLR, and inhibin were augmented, resulting in gonadotropins decline. Interestingly, autophagy biomarkers, Beclin-1, ATG5, ATG12, LC3-II, and LAMP1 were reduced but SQSTM1/p62 was augmented in the ovaries of HFD-HF-fed rats, causing autolysosome to aggregation. The diet altered T, E2, P4, PRL, and their receptors status in the ovary, disturbed estrous cyclicity, and delayed vaginal opening. Ovarian histomorphology exhibited numerous cystic and atretic follicles, along with disturbed follicular maturation and ovulation. Moreover, the reduction of FSHR; steroidogenic proteins; receptor proteins AR, ERβ, PR; and signaling proteins Wnt2 and β-catenin was also noticed in the ovary, whereas PRLR, inhibin, and pGSK3β were augmented. In conclusion, exposure to a prepubertal HFD-HF diet leads to hypogonadotropism and the autophagy-mediated defective differentiation of ovarian follicles, abating fertility in adult rats.

Obesity-related disruptions in female reproduction are a growing concern. The neuroendocrine regulation of female reproduction in the context of obesity involves the intricate interplay between adipokines and the Hypothalamus-Pituitary- Ovarian (HPO ) axis. In this review, we explore the role of adipokines, particularly leptin and adiponectin, in regulating neuroendocrine female reproduction in the context of obesity. Leptin, primarily produced by adipocytes, plays a pivotal role in signaling energy status to the brain. However, excessive levels of obesity can lead to leptin resistance, affecting the HPO axis and causing menstrual irregularities and fertility issues. Adiponectin, on the other hand, is reduced in obesity and influences insulin sensitivity and ovarian function. We delve into the impact of altered adipokine levels on the HPO axis, discussing disruptions in hormone secretion, oocyte maturation, and ovarian steroidogenesis. This study paves the way for further exploration of adipokine-related pathways and potential therapeutic targets, enhancing our understanding of the intricate relationship between obesity and female reproduction.